down regulation of nitric oxide

February 4, 2008

ive just been doing some reading about nitric oxide specifically

endothelial at first.

i dont know about you guys but i seem to be responding occasionally

to sexual thoughts and stimuli now and again.

when i first got pssd the first thing i noticed was getting an

erection was difficult to say the least but when i was with my

girlfriend my penis would still respond sexually but not get fully

erect.

immediately i thought the ssris had done something to my penis.

before pssd i would respond sexually in the same way, there was a

thought of arrousal my penis would get semi erect and that semi erect

state went into an erection without having to think about it.

i.e. after the initial thought and arrousal my mind could wander

elsewhere and think of other things as my penis would look after its

self from there on and get erect.

now with pssd i have to keep with that install thought and keep

thinking and thinking intencly about it beyond the point where before

pssd it would just take over and do the job for me to get an erection.

after reading about erections and understanding the mechanisms

involved it became apparent that it was endothelial nitric oxide that

is released when that initial rush of blood flows in.

the initial rush of blood puts pressure on the endothelial cells

which in turn release nitric oxide. (this is not a theory of mine its

fact)

it seems in my case that the mechanisms involved with endothelial

release of nitric oxide have been altered by the ssri.

this is why getting aroused is so much more difficult, i have think

about it longer and longer for the blood to keep flowing in. i.e my

erections are dependant on the nitric oxide released from the nerves

in the penis to get an erection. (im positive this is the case and

thats why masturbating is so difficult)

ive come across some interesting articles on nitric oxide (links

beleow) and how the nitric oxide system in the body has a negative

feed back inhibition or negative feedback loop.

just like a body builder that takes testosterone gets feed back

inhibition of his own testosterone, it seems nitric oxide synthesis

also has a similar effect.

ive come across an article about paroxetine and how it effects nitric

oxide apparently in some individuals it can increase endothelial

nitric oxide synthesis so when you stop taking it. back down

regulation and possibly pssd!

" the SSRI-induced decrease in platelet serotonin uptake likely

contributes substantially to SSRI-induced decrease in platelet

activity (Serebruany et al, 2003). The decrease of platelet eNOS

activity observed in HCs could be interpreted as a homeostatic

downregulation in response to the paroxetine-induced excessive

increase in NO availability. Indeed, exposure of washed human

platelets to NO has been shown to induce a compensatory decrease in

platelet eNOS activity (Chen and Mehta, 1997). "

http://www.nature.com/npp/journal/v31/n6/full/1300961a.html#bib9

i think its likely that pssd is this effect.

now check this info out!

apparently statins (cholesterol lowering drug) actually increases

endothelial nitric oxide synthesis. however when you discontinue the

statins theres an inhibition of nitric oxide synthesis.

http://circ.ahajournals.org/cgi/content/full/102/25/3104

http://www.medscape.com/viewarticle/563252_2

its reasonable to assume that the same process is happening with

ssri's, why would it not? this could cause pssd.

ive come across this.

" cGMP and nitrite level in the blood serum were measured in patients

with migraine. The group under study included 37 subjects suffering

from migraine with and without aura and 40 normal control subjects.

The cGMP was measured during a migraine attack and 60 min following

the administration of sumatriptan 6 mg subcutaneously. A

statistically significant increase in cGMP level was observed in

patients during a migraine attack compared to the controls. This

level decreased after the administration of sumatriptan, but it was

still higher than in the controls. "

http://www.neurotransmitter.net/migraineno.html

sumatriptan i think increases nitric oxide in the brain and then

lowers after discontinuing but still remains higher than it was at

first.

http://en.wikipedia.org/wiki/Sumatriptan

also found this.

it seems caffeine can inhibit the enzyme arginase, which converts

arginine to ornithine and urea, thus leaving more arginine for nitric

oxide synthesis.

also in this same link below it says that Red Wine Increases

Expression of Human Endothelial Nitric Oxide Syntheses.

" If this effect also occurs in human endothelial cells in vivo, it

would mean that for any given amount of arginine available in the

bloodstream, more arginine would be used by nitric oxide synthase to

produce nitric oxide, thus improving endothelial function. Since

arginase and nitric oxide synthase compete for the common substrate

arginine, there would be less arginine used by the arginase pathway

as compared to that which would occur at a lower level of expression

of nitric oxide synthase. "

http://www.lef.org/dsnews/ds_letter_2004_apr.html

im tempted to drink red wine and a lots of caffeine.

but reading about feed back inhibition of nitric oxide synthesis im

not sure, its a fucking mindfield all this and im sure drug company's

releace false research data to send people barking the wrong tree!

we just all have to be our own guinea pig!

one thinking is for sure though ssris do effect nitric oxide other

wise we wouldn't be here, so i think this down regulation of nitric

oxide synthesis could be the thing thats causes pssd!!!!!!!

February 4, 2008

Wow,

Very informative research, and I agree with you 100%. I can get a

semi-erection now, but I havent had the blood rush tingly feeling

since the pssd hit me. That must be because NO was downregulated in

my brain or penis, not sure which. Any theories on that?

>

> ive just been doing some reading about nitric oxide specifically

> endothelial at first.

>

> i dont know about you guys but i seem to be responding occasionally

> to sexual thoughts and stimuli now and again.

>

> when i first got pssd the first thing i noticed was getting an

> erection was difficult to say the least but when i was with my

> girlfriend my penis would still respond sexually but not get fully

> erect.

>

> immediately i thought the ssris had done something to my penis.

>

> before pssd i would respond sexually in the same way, there was a

> thought of arrousal my penis would get semi erect and that semi erect

> state went into an erection without having to think about it.

>

> i.e. after the initial thought and arrousal my mind could wander

> elsewhere and think of other things as my penis would look after its

> self from there on and get erect.

>

> now with pssd i have to keep with that install thought and keep

> thinking and thinking intencly about it beyond the point where before

> pssd it would just take over and do the job for me to get an erection.

>

> after reading about erections and understanding the mechanisms

> involved it became apparent that it was endothelial nitric oxide that

> is released when that initial rush of blood flows in.

>

> the initial rush of blood puts pressure on the endothelial cells

> which in turn release nitric oxide. (this is not a theory of mine its

> fact)

>

> it seems in my case that the mechanisms involved with endothelial

> release of nitric oxide have been altered by the ssri.

>

> this is why getting aroused is so much more difficult, i have think

> about it longer and longer for the blood to keep flowing in. i.e my

> erections are dependant on the nitric oxide released from the nerves

> in the penis to get an erection. (im positive this is the case and

> thats why masturbating is so difficult)

>

> ive come across some interesting articles on nitric oxide (links

> beleow) and how the nitric oxide system in the body has a negative

> feed back inhibition or negative feedback loop.

>

> just like a body builder that takes testosterone gets feed back

> inhibition of his own testosterone, it seems nitric oxide synthesis

> also has a similar effect.

>

> ive come across an article about paroxetine and how it effects nitric

> oxide apparently in some individuals it can increase endothelial

> nitric oxide synthesis so when you stop taking it. back down

> regulation and possibly pssd!

>

> " the SSRI-induced decrease in platelet serotonin uptake likely

> contributes substantially to SSRI-induced decrease in platelet

> activity (Serebruany et al, 2003). The decrease of platelet eNOS

> activity observed in HCs could be interpreted as a homeostatic

> downregulation in response to the paroxetine-induced excessive

> increase in NO availability. Indeed, exposure of washed human

> platelets to NO has been shown to induce a compensatory decrease in

> platelet eNOS activity (Chen and Mehta, 1997). "

>

> http://www.nature.com/npp/journal/v31/n6/full/1300961a.html#bib9

>

> i think its likely that pssd is this effect.

>

> now check this info out!

>

> apparently statins (cholesterol lowering drug) actually increases

> endothelial nitric oxide synthesis. however when you discontinue the

> statins theres an inhibition of nitric oxide synthesis.

>

> http://circ.ahajournals.org/cgi/content/full/102/25/3104

> http://www.medscape.com/viewarticle/563252_2

>

> its reasonable to assume that the same process is happening with

> ssri's, why would it not? this could cause pssd.

>

> ive come across this.

>

> " cGMP and nitrite level in the blood serum were measured in patients

> with migraine. The group under study included 37 subjects suffering

> from migraine with and without aura and 40 normal control subjects.

> The cGMP was measured during a migraine attack and 60 min following

> the administration of sumatriptan 6 mg subcutaneously. A

> statistically significant increase in cGMP level was observed in

> patients during a migraine attack compared to the controls. This

> level decreased after the administration of sumatriptan, but it was

> still higher than in the controls. "

>

> http://www.neurotransmitter.net/migraineno.html

>

> sumatriptan i think increases nitric oxide in the brain and then

> lowers after discontinuing but still remains higher than it was at

> first.

>

> http://en.wikipedia.org/wiki/Sumatriptan

>

> also found this.

>

> it seems caffeine can inhibit the enzyme arginase, which converts

> arginine to ornithine and urea, thus leaving more arginine for nitric

> oxide synthesis.

>

> also in this same link below it says that Red Wine Increases

> Expression of Human Endothelial Nitric Oxide Syntheses.

>

> " If this effect also occurs in human endothelial cells in vivo, it

> would mean that for any given amount of arginine available in the

> bloodstream, more arginine would be used by nitric oxide synthase to

> produce nitric oxide, thus improving endothelial function. Since

> arginase and nitric oxide synthase compete for the common substrate

> arginine, there would be less arginine used by the arginase pathway

> as compared to that which would occur at a lower level of expression

> of nitric oxide synthase. "

>

> http://www.lef.org/dsnews/ds_letter_2004_apr.html

>

> im tempted to drink red wine and a lots of caffeine.

>

> but reading about feed back inhibition of nitric oxide synthesis im

> not sure, its a fucking mindfield all this and im sure drug company's

> releace false research data to send people barking the wrong tree!

>

> we just all have to be our own guinea pig!

>

> one thinking is for sure though ssris do effect nitric oxide other

> wise we wouldn't be here, so i think this down regulation of nitric

> oxide synthesis could be the thing thats causes pssd!!!!!!!

>

February 4, 2008

i definitely think pssd is nitric oxide related in probably every

way, physical down regulation of endothelial nitric oxide and

possibly down regulation of neural nitric oxide in the brain.

i remeber reading that endothelial nitric oxide also has neurological

effects so is a possibility that its just endothelial coupled with

the effects of enhances in serotonin pathways in the brain from the

ssri use.

the way they have enhanced the serotonin pathways is not in my

opinion any thing to do with neuroregenerative properties as the drug

company's would have us believe but that of a defencive reaction by

the neurons in the brain.

i.e. serotonin is released form neurons and unable to be restored

because the ssri blocks the transporter, the excess that is released

probably gets broken down by monoamine oxidase, thus creating a small

ammount of serotonin in the brain. the neurons probably respond to

this by trying to grow new smaller connections to cope with the loss

and so the can function on less amounts of serotonin, then when you

stop taking them the brain is flooded with serotonin thats converted

from tryptophan in the diet and this is an excess the the new smaller

neurons so there stimulation is constant or at least excessive.

" The mechanism of antidepressant-induced ED appears to be related to

the therapeutic activity of selective serotonin reuptake inhibitors

(SSRIs). One of the main roles of the central nervous system (CNS) in

human sexual response is to suppress erections through the

sympathetic nervous system and a cluster of neurons known as the

paragigantocellular nucleus (PGN). The PGN neurons send signals down

their axons to the erection-generating center in the spine. There the

PGN neurons release serotonin, which acts as a chemical messenger

within the erection-generating center that suppresses erections by

inhibiting the effects of pro-erectile neurotransmitters. (5) As a

result, NO synthase is inhibited and NO release into penile smooth

muscle is reduced. Millions of Americans take SSRI drugs that work in

part by increasing CNS levels of serotonin. It has been proposed

that, by increasing the level of serotonin in the CNS, pro-erectile

physiologic mechanisms are inhibited. "

http://www.encyclopedia.com/doc/1G1-114563485.html

its somthing thats hard to get may head round about what will and

what wont up regulate nitric oxide because of the negative feed back.

one thing i can tell you though is ive tried all sorts of supplements

and one that had an effect on erections was believe it or

not " quercitin " . i couldnt believe it when i saw results from taking

it.

ive researched it and it actually has nitric oxide effects, its

unclear what effect its having but its a positive one for sure, the

majority of what ive read about it says it has inhibitory effects on

endothelial nitric oxide, what ive experienced is the opposite of

this.

(YOU WILL HAVE TO USE SELECT RIGHT MOUSE CLICK COPY AND PAST INTO

ADDRESS BAR TO USE THIS LINK)

http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6WNT-

4NJ20KH-

1 & _user=10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 &

_version=1 & _urlVersion=0 & _userid=10 & md5=47a17690a3224aafafef7509eb0cad

fe

im thinking is it possible that down regulating endotheliail nitric

oxide is actually up regulating the nitric oxide synthesis?

im curious to see the effects of quercetin combined with ginkgo

Biloba.

i took ssri's years ago and didnt get pssd, when i got pssd i was

only taking a very small amount of citalopram half the 10mg pill per

day just less for about two weeks probably 8 pills in total.

now after reading about the effects red wine has on up regulating

nitric oxide it hit me!

i was away just after the time i started to take them with a new

girlfriend sex was fine up until the 3rd or 4th day then it was

really difficult to get an errection and the erections i was getting

were small but sort of hard, like half the size they normally would

be,i have my girlfriend as a witness to this.

i stopped taking the ssri and this continued over a few weeks until i

just couldnt get any errection or be aroused by anything.

now ask me what i had just started drinking the week i was away with

my girlfriend?

RED WINE specifically the french red wine cabernet sauvignon, it ties

in to when the pssd actually happened!

this type of red wine has the highest concentrations of the

ingredients that make it healthy for the heart and also what

increases nitric oxide synthesis and its also the type of red wine

that all the research has been done on for these effects.

if you do a search on " red wine nitric oxide " you will see.

it seems that taking the ssri and having a few classes of red wine is

what caused my pssd, the ssris effects on nitric oxide coupled with

the red wines effects on nitric oxide has probably down regulated

expression of nitric oxide through feedback inhibition. (i never made

the connection untill last night after reading about the effects of

red wine on nitric oxide expression, ive contacted my girlfriend and

shes confirmed that the problem started just after we bought the wine

and what the wine was called) I THINK THIS IS GREAT NEWS!

i think we all need to concentrate and research things that effect

nitric oxide expression.

ive found this patent on something that up regulates nitric oxide.

http://www.patentstorm.us/patents/6180597-description.html

and just to add a bit more about quercitin, ive found some

information about its effects on ca2+ channels.

http://www.cababstractsplus.org/google/abstract.asp?AcNo=20053140757

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1573296

> >

> > ive just been doing some reading about nitric oxide specifically

> > endothelial at first.

> >

> > i dont know about you guys but i seem to be responding

occasionally

> > to sexual thoughts and stimuli now and again.

> >

> > when i first got pssd the first thing i noticed was getting an

> > erection was difficult to say the least but when i was with my

> > girlfriend my penis would still respond sexually but not get

fully

> > erect.

> >

> > immediately i thought the ssris had done something to my penis.

> >

> > before pssd i would respond sexually in the same way, there was a

> > thought of arrousal my penis would get semi erect and that semi

erect

> > state went into an erection without having to think about it.

> >

> > i.e. after the initial thought and arrousal my mind could wander

> > elsewhere and think of other things as my penis would look after

its

> > self from there on and get erect.

> >

> > now with pssd i have to keep with that install thought and keep

> > thinking and thinking intencly about it beyond the point where

before

> > pssd it would just take over and do the job for me to get an

erection.

> >

> > after reading about erections and understanding the mechanisms

> > involved it became apparent that it was endothelial nitric oxide

that

> > is released when that initial rush of blood flows in.

> >

> > the initial rush of blood puts pressure on the endothelial cells

> > which in turn release nitric oxide. (this is not a theory of mine

its

> > fact)

> >

> > it seems in my case that the mechanisms involved with endothelial

> > release of nitric oxide have been altered by the ssri.

> >

> > this is why getting aroused is so much more difficult, i have

think

> > about it longer and longer for the blood to keep flowing in. i.e

my

> > erections are dependant on the nitric oxide released from the

nerves

> > in the penis to get an erection. (im positive this is the case

and

> > thats why masturbating is so difficult)

> >

> > ive come across some interesting articles on nitric oxide (links

> > beleow) and how the nitric oxide system in the body has a

negative

> > feed back inhibition or negative feedback loop.

> >

> > just like a body builder that takes testosterone gets feed back

> > inhibition of his own testosterone, it seems nitric oxide

synthesis

> > also has a similar effect.

> >

> > ive come across an article about paroxetine and how it effects

nitric

> > oxide apparently in some individuals it can increase endothelial

> > nitric oxide synthesis so when you stop taking it. back down

> > regulation and possibly pssd!

> >

> > " the SSRI-induced decrease in platelet serotonin uptake likely

> > contributes substantially to SSRI-induced decrease in platelet

> > activity (Serebruany et al, 2003). The decrease of platelet eNOS

> > activity observed in HCs could be interpreted as a homeostatic

> > downregulation in response to the paroxetine-induced excessive

> > increase in NO availability. Indeed, exposure of washed human

> > platelets to NO has been shown to induce a compensatory decrease

in

> > platelet eNOS activity (Chen and Mehta, 1997). "

> >

> > http://www.nature.com/npp/journal/v31/n6/full/1300961a.html#bib9

> >

> > i think its likely that pssd is this effect.

> >

> > now check this info out!

> >

> > apparently statins (cholesterol lowering drug) actually increases

> > endothelial nitric oxide synthesis. however when you discontinue

the

> > statins theres an inhibition of nitric oxide synthesis.

> >

> > http://circ.ahajournals.org/cgi/content/full/102/25/3104

> > http://www.medscape.com/viewarticle/563252_2

> >

> > its reasonable to assume that the same process is happening with

> > ssri's, why would it not? this could cause pssd.

> >

> > ive come across this.

> >

> > " cGMP and nitrite level in the blood serum were measured in

patients

> > with migraine. The group under study included 37 subjects

suffering

> > from migraine with and without aura and 40 normal control

subjects.

> > The cGMP was measured during a migraine attack and 60 min

following

> > the administration of sumatriptan 6 mg subcutaneously. A

> > statistically significant increase in cGMP level was observed in

> > patients during a migraine attack compared to the controls. This

> > level decreased after the administration of sumatriptan, but it

was

> > still higher than in the controls. "

> >

> > http://www.neurotransmitter.net/migraineno.html

> >

> > sumatriptan i think increases nitric oxide in the brain and then

> > lowers after discontinuing but still remains higher than it was

at

> > first.

> >

> > http://en.wikipedia.org/wiki/Sumatriptan

> >

> > also found this.

> >

> > it seems caffeine can inhibit the enzyme arginase, which converts

> > arginine to ornithine and urea, thus leaving more arginine for

nitric

> > oxide synthesis.

> >

> > also in this same link below it says that Red Wine Increases

> > Expression of Human Endothelial Nitric Oxide Syntheses.

> >

> > " If this effect also occurs in human endothelial cells in vivo,

it

> > would mean that for any given amount of arginine available in the

> > bloodstream, more arginine would be used by nitric oxide synthase

to

> > produce nitric oxide, thus improving endothelial function. Since

> > arginase and nitric oxide synthase compete for the common

substrate

> > arginine, there would be less arginine used by the arginase

pathway

> > as compared to that which would occur at a lower level of

expression

> > of nitric oxide synthase. "

> >

> > http://www.lef.org/dsnews/ds_letter_2004_apr.html

> >

> > im tempted to drink red wine and a lots of caffeine.

> >

> > but reading about feed back inhibition of nitric oxide synthesis

im

> > not sure, its a fucking mindfield all this and im sure drug

company's

> > releace false research data to send people barking the wrong tree!

> >

> > we just all have to be our own guinea pig!

> >

> > one thinking is for sure though ssris do effect nitric oxide

other

> > wise we wouldn't be here, so i think this down regulation of

nitric

> > oxide synthesis could be the thing thats causes pssd!!!!!!!

> >

>

February 6, 2008

ive got some more to add to this subject, ive found that vitamin c,

fish oils, polyunsaturated fatty acids and folic acid effect nitric

oxide synthesis.

http://www.jbc.org/cgi/content/full/274/12/8254

http://circ.ahajournals.org/cgi/content/abstract/104/10/1119

http://circ.ahajournals.org/cgi/content/short/CIRCULATIONAHA.106.67908

4v1

http://lansbury.bwh.harvard.edu/pufas_and_nitric_oxide_(NO).htm

also found this about Tetrahydrobiopterin,its a co-factor needed for

nitric oxide synthesis.

http://www.life-enhancement.com/le/article_template.asp?ID=841

http://en.wikipedia.org/wiki/Tetrahydrobiopterin

> > >

> > > ive just been doing some reading about nitric oxide

specifically

> > > endothelial at first.

> > >

> > > i dont know about you guys but i seem to be responding

> occasionally

> > > to sexual thoughts and stimuli now and again.

> > >

> > > when i first got pssd the first thing i noticed was getting an

> > > erection was difficult to say the least but when i was with my

> > > girlfriend my penis would still respond sexually but not get

> fully

> > > erect.

> > >

> > > immediately i thought the ssris had done something to my penis.

> > >

> > > before pssd i would respond sexually in the same way, there was

a

> > > thought of arrousal my penis would get semi erect and that semi

> erect

> > > state went into an erection without having to think about it.

> > >

> > > i.e. after the initial thought and arrousal my mind could

wander

> > > elsewhere and think of other things as my penis would look

after

> its

> > > self from there on and get erect.

> > >

> > > now with pssd i have to keep with that install thought and keep

> > > thinking and thinking intencly about it beyond the point where

> before

> > > pssd it would just take over and do the job for me to get an

> erection.

> > >

> > > after reading about erections and understanding the mechanisms

> > > involved it became apparent that it was endothelial nitric

oxide

> that

> > > is released when that initial rush of blood flows in.

> > >

> > > the initial rush of blood puts pressure on the endothelial

cells

> > > which in turn release nitric oxide. (this is not a theory of

mine

> its

> > > fact)

> > >

> > > it seems in my case that the mechanisms involved with

endothelial

> > > release of nitric oxide have been altered by the ssri.

> > >

> > > this is why getting aroused is so much more difficult, i have

> think

> > > about it longer and longer for the blood to keep flowing in.

i.e

> my

> > > erections are dependant on the nitric oxide released from the

> nerves

> > > in the penis to get an erection. (im positive this is the case

> and

> > > thats why masturbating is so difficult)

> > >

> > > ive come across some interesting articles on nitric oxide

(links

> > > beleow) and how the nitric oxide system in the body has a

> negative

> > > feed back inhibition or negative feedback loop.

> > >

> > > just like a body builder that takes testosterone gets feed back

> > > inhibition of his own testosterone, it seems nitric oxide

> synthesis

> > > also has a similar effect.

> > >

> > > ive come across an article about paroxetine and how it effects

> nitric

> > > oxide apparently in some individuals it can increase

endothelial

> > > nitric oxide synthesis so when you stop taking it. back down

> > > regulation and possibly pssd!

> > >

> > > " the SSRI-induced decrease in platelet serotonin uptake likely

> > > contributes substantially to SSRI-induced decrease in platelet

> > > activity (Serebruany et al, 2003). The decrease of platelet

eNOS

> > > activity observed in HCs could be interpreted as a homeostatic

> > > downregulation in response to the paroxetine-induced excessive

> > > increase in NO availability. Indeed, exposure of washed human

> > > platelets to NO has been shown to induce a compensatory

decrease

> in

> > > platelet eNOS activity (Chen and Mehta, 1997). "

> > >

http://www.nature.com/npp/journal/v31/n6/full/1300961a.html#bib9

> > >

> > > i think its likely that pssd is this effect.

> > >

> > > now check this info out!

> > >

> > > apparently statins (cholesterol lowering drug) actually

increases

> > > endothelial nitric oxide synthesis. however when you

discontinue

> the

> > > statins theres an inhibition of nitric oxide synthesis.

> > >

> > > http://circ.ahajournals.org/cgi/content/full/102/25/3104

> > > http://www.medscape.com/viewarticle/563252_2

> > >

> > > its reasonable to assume that the same process is happening

with

> > > ssri's, why would it not? this could cause pssd.

> > >

> > > ive come across this.

> > >

> > > " cGMP and nitrite level in the blood serum were measured in

> patients

> > > with migraine. The group under study included 37 subjects

> suffering

> > > from migraine with and without aura and 40 normal control

> subjects.

> > > The cGMP was measured during a migraine attack and 60 min

> following

> > > the administration of sumatriptan 6 mg subcutaneously. A

> > > statistically significant increase in cGMP level was observed

in

> > > patients during a migraine attack compared to the controls.

This

> > > level decreased after the administration of sumatriptan, but it

> was

> > > still higher than in the controls. "

> > >

> > > http://www.neurotransmitter.net/migraineno.html

> > >

> > > sumatriptan i think increases nitric oxide in the brain and

then

> > > lowers after discontinuing but still remains higher than it was

> at

> > > first.

> > >

> > > http://en.wikipedia.org/wiki/Sumatriptan

> > >

> > > also found this.

> > >

> > > it seems caffeine can inhibit the enzyme arginase, which

converts

> > > arginine to ornithine and urea, thus leaving more arginine for

> nitric

> > > oxide synthesis.

> > >

> > > also in this same link below it says that Red Wine Increases

> > > Expression of Human Endothelial Nitric Oxide Syntheses.

> > >

> > > " If this effect also occurs in human endothelial cells in vivo,

> it

> > > would mean that for any given amount of arginine available in

the

> > > bloodstream, more arginine would be used by nitric oxide

synthase

> to

> > > produce nitric oxide, thus improving endothelial function.

Since

> > > arginase and nitric oxide synthase compete for the common

> substrate

> > > arginine, there would be less arginine used by the arginase

> pathway

> > > as compared to that which would occur at a lower level of

> expression

> > > of nitric oxide synthase. "

> > >

> > > http://www.lef.org/dsnews/ds_letter_2004_apr.html

> > >

> > > im tempted to drink red wine and a lots of caffeine.

> > >

> > > but reading about feed back inhibition of nitric oxide

synthesis

> im

> > > not sure, its a fucking mindfield all this and im sure drug

> company's

> > > releace false research data to send people barking the wrong

tree!

> > >

> > > we just all have to be our own guinea pig!

> > >

> > > one thinking is for sure though ssris do effect nitric oxide

> other

> > > wise we wouldn't be here, so i think this down regulation of

> nitric

> > > oxide synthesis could be the thing thats causes pssd!!!!!!!

> > >

> >

>

February 12, 2008

I've read somewhere that one of the possible problems with ssris is

that they also cause less NO to be sent to the genitals.

Generally when you get an erection you get initiall stimulation that

then signals an initiall " rush " of nitric oxide.

It is possible that ssris stop that stimulation, or weaken it.

That stuff I got, Nitro FX does seem to have made a few improvements.

However, I fear that what is stopping NO from signalling may be more

complex.

I think it probably relates back to the parts of the brain that are

responsible for emotional processing, such as dopamine, adrenaline,

mascurinic, nicotinic.

If you can lose your ability to cry completely, then such

disturbances are likely.

Such problems are likely to cause complex problems with sexual

stimulation, and thereby stop the initial rush of NO.

On top of that, I assume the stress and depression associated with

poor levels of serotonin aggrivates the problem.

February 13, 2008

ive read that its serotonin that blocks the releace of nitric oxide

in the genitals.

but down regulation of nitric oxide is also something that could

cause pssd.

>

> I've read somewhere that one of the possible problems with ssris is

> that they also cause less NO to be sent to the genitals.

>

> Generally when you get an erection you get initiall stimulation

that

> then signals an initiall " rush " of nitric oxide.

>

> It is possible that ssris stop that stimulation, or weaken it.

>

> That stuff I got, Nitro FX does seem to have made a few

improvements.

>

> However, I fear that what is stopping NO from signalling may be

more

> complex.

>

> I think it probably relates back to the parts of the brain that are

> responsible for emotional processing, such as dopamine, adrenaline,

> mascurinic, nicotinic.

>

> If you can lose your ability to cry completely, then such

> disturbances are likely.

>

> Such problems are likely to cause complex problems with sexual

> stimulation, and thereby stop the initial rush of NO.

>

> On top of that, I assume the stress and depression associated with

> poor levels of serotonin aggrivates the problem.

>

February 14, 2008

I think the process is extremely complicated, and there is probably

something that we are missing out. One thing that we should bear in

mind is - most people with pssd don't have cardiovuscular problems

(or at least not that I have heard of). I have had my blood pressure

checked several times and this appears to be so.

Therefore, it is unlikey that we are " not producing enough nitric

oxide. " But I believe that it is likely that it is not " signilling

properly. "

In my perosnal experience, serotonin levels is less of an issue than

people make it out to be.

Sleep deprivation raises serotonin massively, this is one of the

reaosns that it has an antidepressant effect.

Also, MDMA raises serotonin, and afterwards causes it to drop. It

generally when the serotonin was dropping that I had erections though.

There are several complex processes involved in nitric oxide

signalling, or so I believe.

One important enzyme is " tyrosine kinase. "

dopamine stimulates this enzyme

" increase in dopamine (DA) availability in rat brain has been

suggested to participate in certain neurodegenerative processes.

However, the regulatory effects of DA on glial cells have not been

extensively studied. Using a rat C6 glioma cell line stably

expressing recombinant D2L receptors, we have found that micromolar

levels of DA stimulate mitogenesis and glial fibrillary acidic

protein (GFAP) expression, both serving as parameters of reactive

gliosis. This mitogenesis occurs about 29 h after exposure to DA and

requires D2-receptor-mediated intracellular redox-tyrosine kinase

activation. Either DA or quinpirole, a D2 receptor agonist,

stimulates protein tyrosine phosphorylation. Application of either

DPI, a potent inhibitor of NADPH-dependent oxidase, or NAC, an anti-

oxidant, effectively prevented DA-induced tyrosine phosphorylation

and DNA synthesis. Preincubation of (+)-butaclamol, a D2 receptor

antagonist, inhibits both DA-stimulated tyrosine phosphorylation and

mitogenesis. DA at micromolar levels also stimulates GFAP expression.

This DA-regulated GFAP expression can be completely inhibited by

SB203580, a selective p38 MAPK inhibitor, but not influenced by (+)-

butaclamol and genistein, a protein tyrosine kinase inhibitor. Thus,

our data suggest that regulation of DNA synthesis and GFAP expression

induced by DA is mediated by independent signaling pathways. The

mitogenesis requires a D2-receptor-mediated protein tyrosine kinase

cascade, while GFAP expression needs a D2-receptor-independent p38

MAPK activation. This observation may help to understand the

processes of reactive gliosis in some dopaminergic-related

neurodegenerative diseases. "

Tyrosine Kinase, in turn helps to enhance the " signalling process " of

another enzyme called Guanylyl cyclase c.

" Guanylyl cyclase c, or GC-C, is an enzyme found only in the luminal

aspect of intestinal epithelium. The receptor has an extracellular

ligand-binding domain, a single transmembrane region, a region with

sequence similar to that of protein kinases, and a C-terminal

guanylyl cyclase domain. Tyrosine kinase activity mediates the GC-C

signaling pathway within the cell. "

In turn, this molecule is very important for " signalling " NO

Nitric oxide (NO)-sensitive guanylyl cyclase (NO-sensitive GC) is

generally accepted as the most important receptor for the signaling

molecule NO. This enzyme is also known as soluble or cytosolic GC, a

designation chosen to distinguish the enzyme from its membrane-bound

counterpart. Because recently one of the isoforms of the " soluble " GC

has been found to associate with the cell membrane, we will use the

term " NO-sensitive " GC throughout this review. Here is a link for you

to read, i don't really understand it properly.

http://circres.ahajournals.org/cgi/content/full/93/2/96

As I expected the D2 receptors seem to play an important role in this

signalling. To be honset this is an area that is really complex. I

think we will have to keep thinking about this problem before we come

up with a specific answer.

I still believe that it is the process of arousal that is interfered

with. I believe that Nitric Oxide is involved (otherwise why would I

not get erections during sleep etc).

February 15, 2008

I think it is more complicated than that. Serotonin blocks NO in

certain parts of the brain. Some ssris raise Nitric Oxide, whilst some

of them lower nitric oxide. Stablon actually downgrades NO did you know

that? I think the link between serotonin and No is tenuous. And also,

in order to get any good out of it you would have to have a better

understanding of what we should be doing to serotnin.

I keep coming back to the inability to cry, because that is a problem

with the muscles behind the eyes. You can see that this is also causing

problems with blurred vision etc.

I think there are problems with that whole part of the nervous system:

Muscarinic

Nicotinin

Dopamine signalling

Nitric Oxide signalling.

February 15, 2008

serotonin is synthesised into melatonin at night when you get tired

so i dont think tiredness increases serotonin.

it could be this decrease that brings about the sleep deprived

recovery by not having the serotonin suppress the nitric oxide.

i get erections through the night, but still cant get one through

anything visual or kissing or touching. i seem to respond to

suggestion occasionally in a normal way. i.e reading something like a

txt conversation that turns towards the idea of sex with a girlfriend.

this is actually a nightmare because i feel turned to take things

further but i know when the situation arises i wont get turned on

because the suggestion part of the arousal is over.

>

> I think the process is extremely complicated, and there is probably

> something that we are missing out. One thing that we should bear in

> mind is - most people with pssd don't have cardiovuscular problems

> (or at least not that I have heard of). I have had my blood

pressure

> checked several times and this appears to be so.

>

> Therefore, it is unlikey that we are " not producing enough nitric

> oxide. " But I believe that it is likely that it is not " signilling

> properly. "

>

> In my perosnal experience, serotonin levels is less of an issue

than

> people make it out to be.

>

> Sleep deprivation raises serotonin massively, this is one of the

> reaosns that it has an antidepressant effect.

>

> Also, MDMA raises serotonin, and afterwards causes it to drop. It

> generally when the serotonin was dropping that I had erections

though.

>

> There are several complex processes involved in nitric oxide

> signalling, or so I believe.

>

> One important enzyme is " tyrosine kinase. "

>

> dopamine stimulates this enzyme

>

> " increase in dopamine (DA) availability in rat brain has been

> suggested to participate in certain neurodegenerative processes.

> However, the regulatory effects of DA on glial cells have not been

> extensively studied. Using a rat C6 glioma cell line stably

> expressing recombinant D2L receptors, we have found that micromolar

> levels of DA stimulate mitogenesis and glial fibrillary acidic

> protein (GFAP) expression, both serving as parameters of reactive

> gliosis. This mitogenesis occurs about 29 h after exposure to DA

and

> requires D2-receptor-mediated intracellular redox-tyrosine kinase

> activation. Either DA or quinpirole, a D2 receptor agonist,

> stimulates protein tyrosine phosphorylation. Application of either

> DPI, a potent inhibitor of NADPH-dependent oxidase, or NAC, an anti-

> oxidant, effectively prevented DA-induced tyrosine phosphorylation

> and DNA synthesis. Preincubation of (+)-butaclamol, a D2 receptor

> antagonist, inhibits both DA-stimulated tyrosine phosphorylation

and

> mitogenesis. DA at micromolar levels also stimulates GFAP

expression.

> This DA-regulated GFAP expression can be completely inhibited by

> SB203580, a selective p38 MAPK inhibitor, but not influenced by (+)-

> butaclamol and genistein, a protein tyrosine kinase inhibitor.

Thus,

> our data suggest that regulation of DNA synthesis and GFAP

expression

> induced by DA is mediated by independent signaling pathways. The

> mitogenesis requires a D2-receptor-mediated protein tyrosine kinase

> cascade, while GFAP expression needs a D2-receptor-independent p38

> MAPK activation. This observation may help to understand the

> processes of reactive gliosis in some dopaminergic-related

> neurodegenerative diseases. "

>

> Tyrosine Kinase, in turn helps to enhance the " signalling process "

of

> another enzyme called Guanylyl cyclase c.

>

> " Guanylyl cyclase c, or GC-C, is an enzyme found only in the

luminal

> aspect of intestinal epithelium. The receptor has an extracellular

> ligand-binding domain, a single transmembrane region, a region with

> sequence similar to that of protein kinases, and a C-terminal

> guanylyl cyclase domain. Tyrosine kinase activity mediates the GC-C

> signaling pathway within the cell. "

>

> In turn, this molecule is very important for " signalling " NO

>

> Nitric oxide (NO)-sensitive guanylyl cyclase (NO-sensitive GC) is

> generally accepted as the most important receptor for the signaling

> molecule NO. This enzyme is also known as soluble or cytosolic GC,

a

> designation chosen to distinguish the enzyme from its membrane-

bound

> counterpart. Because recently one of the isoforms of the " soluble "

GC

> has been found to associate with the cell membrane, we will use the

> term " NO-sensitive " GC throughout this review. Here is a link for

you

> to read, i don't really understand it properly.

>

> http://circres.ahajournals.org/cgi/content/full/93/2/96

>

> As I expected the D2 receptors seem to play an important role in

this

> signalling. To be honset this is an area that is really complex. I

> think we will have to keep thinking about this problem before we

come

> up with a specific answer.

>

> I still believe that it is the process of arousal that is

interfered

> with. I believe that Nitric Oxide is involved (otherwise why would

I

> not get erections during sleep etc).

>

February 15, 2008

you think that there are problems with that part of the nervous

system but you dont think its changes in serotonin pathways that are

instigating those problems.

i didnt know that stablon down regulates nitric oxide but i presumed

it might as it increases uptake of serotonin via an unknown pathway

thought be independent of sert.

quercetin also down regulates nitric oxide, im still taking it every

day and seem to have got a bit better.

ive not started stablon yet.

>

> I think it is more complicated than that. Serotonin blocks NO in

> certain parts of the brain. Some ssris raise Nitric Oxide, whilst

some

> of them lower nitric oxide. Stablon actually downgrades NO did you

know

> that? I think the link between serotonin and No is tenuous. And

also,

> in order to get any good out of it you would have to have a better

> understanding of what we should be doing to serotnin.

>

> I keep coming back to the inability to cry, because that is a

problem

> with the muscles behind the eyes. You can see that this is also

causing

> problems with blurred vision etc.

>

> I think there are problems with that whole part of the nervous

system:

> Muscarinic

> Nicotinin

> Dopamine signalling

> Nitric Oxide signalling.

>

February 16, 2008

This is the point I am trying to make, and if you think about it this

makes sense:

If we were not producing enough of the blood cell form of NO, we

would all have serious cardiovuscular problems by now eg. slow

hearts, hardening of the arteries. I don't think that this is an

occurance in people with PSSD.

It is more likley that the signalling system that causes the rush of

NO when you are aroused is disturbed at one level.

I am triyng to investigate this area further because it is very

complex, and needs more time to be spent on it.

Essentially though, this system has 3 levles. It is most closely

linked to dopamine, but it could also be a disturbance at another

level eg. the gene tyrosine kinase.

That drug that you were taking (melatonin 2?). I think what that does

is agonises tyrosine kinase. That's why you can get erections whilst

on it. It enhances the signalling system which causes NO to rush to

the genitals.

This may also why some people (such as me) sometimes have difficulty

crying. I beleive that the smae system is closely linked with the

nicotinic and muscarinic system.

I believe that MDMA has some similar properties, and amphetamine does

as well. I would need to do more research to find out exactly how

this process works. I think in both drugs it is more complex than

most scientists belive.

I will try to find more articles on this over the next few weeks.

What you have to bear in mind is that this area of knowledge is

beyond most doctors.

February 16, 2008

I don't even get night erections. I keep telling this to my retarded

GPs. All of them say the same things:

" If we have tested you for testosterone and diabetes, then everything

is Ok at the physical end. That means it must be an emotional

problem. "

" There is a lot of rubbish on the internet, most of it is from

adverts from American companies. The things you are reading about

PSSD is probably that. "

" This is what we call life stresses. "

-- In SSRIsex , " nemo.shark " wrote:

>

> serotonin is synthesised into melatonin at night when you get tired

> so i dont think tiredness increases serotonin.

>

> it could be this decrease that brings about the sleep deprived

> recovery by not having the serotonin suppress the nitric oxide.

>

> i get erections through the night, but still cant get one through

> anything visual or kissing or touching. i seem to respond to

> suggestion occasionally in a normal way. i.e reading something like

a

> txt conversation that turns towards the idea of sex with a

girlfriend.

>

> this is actually a nightmare because i feel turned to take things

> further but i know when the situation arises i wont get turned on

> because the suggestion part of the arousal is over.

>

> >

> > I think the process is extremely complicated, and there is

probably

> > something that we are missing out. One thing that we should bear

in

> > mind is - most people with pssd don't have cardiovuscular

problems

> > (or at least not that I have heard of). I have had my blood

> pressure

> > checked several times and this appears to be so.

> >

> > Therefore, it is unlikey that we are " not producing enough nitric

> > oxide. " But I believe that it is likely that it is

not " signilling

> > properly. "

> >

> > In my perosnal experience, serotonin levels is less of an issue

> than

> > people make it out to be.

> >

> > Sleep deprivation raises serotonin massively, this is one of the

> > reaosns that it has an antidepressant effect.

> >

> > Also, MDMA raises serotonin, and afterwards causes it to drop. It

> > generally when the serotonin was dropping that I had erections

> though.

> >

> > There are several complex processes involved in nitric oxide

> > signalling, or so I believe.

> >

> > One important enzyme is " tyrosine kinase. "

> >

> > dopamine stimulates this enzyme

> >

> > " increase in dopamine (DA) availability in rat brain has been

> > suggested to participate in certain neurodegenerative processes.

> > However, the regulatory effects of DA on glial cells have not

been

> > extensively studied. Using a rat C6 glioma cell line stably

> > expressing recombinant D2L receptors, we have found that

micromolar

> > levels of DA stimulate mitogenesis and glial fibrillary acidic

> > protein (GFAP) expression, both serving as parameters of reactive

> > gliosis. This mitogenesis occurs about 29 h after exposure to DA

> and

> > requires D2-receptor-mediated intracellular redox-tyrosine kinase

> > activation. Either DA or quinpirole, a D2 receptor agonist,

> > stimulates protein tyrosine phosphorylation. Application of

either

> > DPI, a potent inhibitor of NADPH-dependent oxidase, or NAC, an

anti-

> > oxidant, effectively prevented DA-induced tyrosine

phosphorylation

> > and DNA synthesis. Preincubation of (+)-butaclamol, a D2 receptor

> > antagonist, inhibits both DA-stimulated tyrosine phosphorylation

> and

> > mitogenesis. DA at micromolar levels also stimulates GFAP

> expression.

> > This DA-regulated GFAP expression can be completely inhibited by

> > SB203580, a selective p38 MAPK inhibitor, but not influenced by

(+)-

> > butaclamol and genistein, a protein tyrosine kinase inhibitor.

> Thus,

> > our data suggest that regulation of DNA synthesis and GFAP

> expression

> > induced by DA is mediated by independent signaling pathways. The

> > mitogenesis requires a D2-receptor-mediated protein tyrosine

kinase

> > cascade, while GFAP expression needs a D2-receptor-independent

p38

> > MAPK activation. This observation may help to understand the

> > processes of reactive gliosis in some dopaminergic-related

> > neurodegenerative diseases. "

> >

> > Tyrosine Kinase, in turn helps to enhance the " signalling

process "

> of

> > another enzyme called Guanylyl cyclase c.

> >

> > " Guanylyl cyclase c, or GC-C, is an enzyme found only in the

> luminal

> > aspect of intestinal epithelium. The receptor has an

extracellular

> > ligand-binding domain, a single transmembrane region, a region

with

> > sequence similar to that of protein kinases, and a C-terminal

> > guanylyl cyclase domain. Tyrosine kinase activity mediates the GC-

C

> > signaling pathway within the cell. "

> >

> > In turn, this molecule is very important for " signalling " NO

> >

> > Nitric oxide (NO)-sensitive guanylyl cyclase (NO-sensitive GC) is

> > generally accepted as the most important receptor for the

signaling

> > molecule NO. This enzyme is also known as soluble or cytosolic

GC,

> a

> > designation chosen to distinguish the enzyme from its membrane-

> bound

> > counterpart. Because recently one of the isoforms of

the " soluble "

> GC

> > has been found to associate with the cell membrane, we will use

the

> > term " NO-sensitive " GC throughout this review. Here is a link for

> you

> > to read, i don't really understand it properly.

> >

> > http://circres.ahajournals.org/cgi/content/full/93/2/96

> >

> > As I expected the D2 receptors seem to play an important role in

> this

> > signalling. To be honset this is an area that is really complex.

I

> > think we will have to keep thinking about this problem before we

> come

> > up with a specific answer.

> >

> > I still believe that it is the process of arousal that is

> interfered

> > with. I believe that Nitric Oxide is involved (otherwise why

would

> I

> > not get erections during sleep etc).

> >

>

February 16, 2008

Here are the articles on the Nitric Oxide signalling system.

n.b Nemo, these are the articles that you wanted to see. I think they

might shed some light onto PSSD, and as to why melatonin 2 helps to

alleviate PSSD. You have to read all these articles in order.

http://www.ingentaconnect.com/content/els/00068993/1999/00000850/0000000

1/art02021;jsessionid=153pbjw5c3iuf.alice?format=print

Guanylyl cyclase c - Wikipedia, the free encyclopedia

http://circres.ahajournals.org/cgi/content/full/93/2/96

February 17, 2008

print the case reports off and take them with you to your doctor and

print the experiments done on rats that got pssd.

doctors are simplistic in there thinking, they think if someone has a

psychological symptom then it must be psychological. they arnt going

to say anything but to you anyway, even if they believe you or that

pssd exists what can they do for you?

nothing, so it will just be like banging your head against a brick

wall.

> > >

> > > I think the process is extremely complicated, and there is

> probably

> > > something that we are missing out. One thing that we should

bear

> in

> > > mind is - most people with pssd don't have cardiovuscular

> problems

> > > (or at least not that I have heard of). I have had my blood

> > pressure

> > > checked several times and this appears to be so.

> > >

> > > Therefore, it is unlikey that we are " not producing enough

nitric

> > > oxide. " But I believe that it is likely that it is

> not " signilling

> > > properly. "

> > >

> > > In my perosnal experience, serotonin levels is less of an issue

> > than

> > > people make it out to be.

> > >

> > > Sleep deprivation raises serotonin massively, this is one of

the

> > > reaosns that it has an antidepressant effect.

> > >

> > > Also, MDMA raises serotonin, and afterwards causes it to drop.

It

> > > generally when the serotonin was dropping that I had erections

> > though.

> > >

> > > There are several complex processes involved in nitric oxide

> > > signalling, or so I believe.

> > >

> > > One important enzyme is " tyrosine kinase. "

> > >

> > > dopamine stimulates this enzyme

> > >

> > > " increase in dopamine (DA) availability in rat brain has been

> > > suggested to participate in certain neurodegenerative

processes.

> > > However, the regulatory effects of DA on glial cells have not

> been

> > > extensively studied. Using a rat C6 glioma cell line stably

> > > expressing recombinant D2L receptors, we have found that

> micromolar

> > > levels of DA stimulate mitogenesis and glial fibrillary acidic

> > > protein (GFAP) expression, both serving as parameters of

reactive

> > > gliosis. This mitogenesis occurs about 29 h after exposure to

DA

> > and

> > > requires D2-receptor-mediated intracellular redox-tyrosine

kinase

> > > activation. Either DA or quinpirole, a D2 receptor agonist,

> > > stimulates protein tyrosine phosphorylation. Application of

> either

> > > DPI, a potent inhibitor of NADPH-dependent oxidase, or NAC, an

> anti-

> > > oxidant, effectively prevented DA-induced tyrosine

> phosphorylation

> > > and DNA synthesis. Preincubation of (+)-butaclamol, a D2

receptor

> > > antagonist, inhibits both DA-stimulated tyrosine

phosphorylation

> > and

> > > mitogenesis. DA at micromolar levels also stimulates GFAP

> > expression.

> > > This DA-regulated GFAP expression can be completely inhibited

by

> > > SB203580, a selective p38 MAPK inhibitor, but not influenced by

> (+)-

> > > butaclamol and genistein, a protein tyrosine kinase inhibitor.

> > Thus,

> > > our data suggest that regulation of DNA synthesis and GFAP

> > expression

> > > induced by DA is mediated by independent signaling pathways.

The

> > > mitogenesis requires a D2-receptor-mediated protein tyrosine

> kinase

> > > cascade, while GFAP expression needs a D2-receptor-independent

> p38

> > > MAPK activation. This observation may help to understand the

> > > processes of reactive gliosis in some dopaminergic-related

> > > neurodegenerative diseases. "

> > >

> > > Tyrosine Kinase, in turn helps to enhance the " signalling

> process "

> > of

> > > another enzyme called Guanylyl cyclase c.

> > >

> > > " Guanylyl cyclase c, or GC-C, is an enzyme found only in the

> > luminal

> > > aspect of intestinal epithelium. The receptor has an

> extracellular

> > > ligand-binding domain, a single transmembrane region, a region

> with

> > > sequence similar to that of protein kinases, and a C-terminal

> > > guanylyl cyclase domain. Tyrosine kinase activity mediates the

GC-

> C

> > > signaling pathway within the cell. "

> > >

> > > In turn, this molecule is very important for " signalling " NO

> > >

> > > Nitric oxide (NO)-sensitive guanylyl cyclase (NO-sensitive GC)

is

> > > generally accepted as the most important receptor for the

> signaling

> > > molecule NO. This enzyme is also known as soluble or cytosolic

> GC,

> > a

> > > designation chosen to distinguish the enzyme from its membrane-

> > bound

> > > counterpart. Because recently one of the isoforms of

> the " soluble "

> > GC

> > > has been found to associate with the cell membrane, we will use

> the

> > > term " NO-sensitive " GC throughout this review. Here is a link

for

> > you

> > > to read, i don't really understand it properly.

> > >

> > > http://circres.ahajournals.org/cgi/content/full/93/2/96

> > >

> > > As I expected the D2 receptors seem to play an important role

in

> > this

> > > signalling. To be honset this is an area that is really

complex.

> I

> > > think we will have to keep thinking about this problem before

we

> > come

> > > up with a specific answer.

> > >

> > > I still believe that it is the process of arousal that is

> > interfered

> > > with. I believe that Nitric Oxide is involved (otherwise why

> would

> > I

> > > not get erections during sleep etc).

> > >

> >

>

February 17, 2008

its melanotan 2 not melatonin, couldnt get that first like up but ive

read the other, it seems that no synthesis can be desensitised and

sensitised.

but i still think its probably more likely that its serotonin

suppressing nitric oxide in the brain, possibly by desensitising.

>

> Here are the articles on the Nitric Oxide signalling system.

>

> n.b Nemo, these are the articles that you wanted to see. I think

they

> might shed some light onto PSSD, and as to why melatonin 2 helps to

> alleviate PSSD. You have to read all these articles in order.

>

http://www.ingentaconnect.com/content/els/00068993/1999/00000850/00000

00

> 1/art02021;jsessionid=153pbjw5c3iuf.alice?format=print

>

> Guanylyl cyclase c - Wikipedia, the free encyclopedia

>

> http://circres.ahajournals.org/cgi/content/full/93/2/96

>

February 17, 2008

its neural nitric oxide that i think has been disrupted or more

precisely down regulated, ether from suppression by serotonin or

changes in expression.

>

> This is the point I am trying to make, and if you think about it

this

> makes sense:

>

> If we were not producing enough of the blood cell form of NO, we

> would all have serious cardiovuscular problems by now eg. slow

> hearts, hardening of the arteries. I don't think that this is an

> occurance in people with PSSD.

>

> It is more likley that the signalling system that causes the rush

of

> NO when you are aroused is disturbed at one level.

>

> I am triyng to investigate this area further because it is very

> complex, and needs more time to be spent on it.

>

> Essentially though, this system has 3 levles. It is most closely

> linked to dopamine, but it could also be a disturbance at another

> level eg. the gene tyrosine kinase.

>

> That drug that you were taking (melatonin 2?). I think what that

does

> is agonises tyrosine kinase. That's why you can get erections

whilst

> on it. It enhances the signalling system which causes NO to rush to

> the genitals.

>

> This may also why some people (such as me) sometimes have

difficulty

> crying. I beleive that the smae system is closely linked with the

> nicotinic and muscarinic system.

>

> I believe that MDMA has some similar properties, and amphetamine

does

> as well. I would need to do more research to find out exactly how

> this process works. I think in both drugs it is more complex than

> most scientists belive.

>

> I will try to find more articles on this over the next few weeks.

> What you have to bear in mind is that this area of knowledge is

> beyond most doctors.

>

February 18, 2008

I think you're missing the point. A lot of doctors say that " nitric

oxide is the key to erections " or something like that.

Actually there are many chemicals involved - dopamine, serotonin,

gaba, oxytopin, histamines, testosterone, acetylcholine,

norepherephine, and adrenaline of course.

I think nitric oxide IS definetely a problem in pssd. However, the

thing about niric oxide is that it isn't nitric oxide that causes

erections really. Nitric oxide just causes the blood vessles to

relax, making it easier to get an erection.

I have tried things like amyl nitrate and levitra, and I'm sure you

have tried cialis etc. These chemicals make it easier to maintain an

erection. However, they do not really work. From what I have been

reading recetly, cialis etc, directly signal nitric oxide to enter

the penis. This helps to enhance erectiosn, but that's about it.

I think you make too much of the connection with serotonin. There are

lots of things that influence nitric oxide, and the main things are

histamines, l-argine etc. The idea that people with high serotonin

have low NO, and vice cersa is too simplistic. For instance, you told

me that eating chocolate would lower NO levels because it raises

serotonin. It probably does raise serotonin, but if you look around

you'll see that it also raises NO levels, so much so that some people

eat it for heart disease!

PSSD probably causes a number of chemical imbalances. The hardest

one's to correct are where certain transmittors are not " signalling "

properly I believe. I think this could be a problem with genes,

proteins, enzymes etc.

However, MDMA did work for me. I think this shows that people with

PSSD could get better with the right chemicals.

I feel like I have a good understanding of how arousal works now.

You need a good amount of chemicals that give you the more " orgasmic "

sort of feelings and get rid of the numbeness etc. I think this

propbably includes GABA, dopamine, norepherephine, oxytopin and

possibly acetylcholine.

I think what actually causes the reection to take place is increased

blood flow to the penis. This is caused by excitement. Sexual

excitement is caused mainly by things like dopamine, oxytopin and

norepherephine I think. Adrenaline causes blood flow to increase.

Also I have noticed that acetylcholine probably helps you to ralax,

thus helping at this stage.

And of course, your blood vessels need to relaxe, thus causing the

blood to enter, and stay in etc. This is a rush of nitric oxide,

aminly caused by dopamine etc. It is possible that other things are

involved such as acetylcholine involved.

I think where you need to start, is by improving your dopamine

suppliments. Vitamin B and fish oils is ok, but really not a very

strong intake. At the moment I am taking l-phenalenaline, vit B6,

magnesium, zinc, vitamin C, niacin, and folic acids. All of those are

needed to convert dopamine. However, dopamine is really difficult to

convert. Most people have found that Mucuna Pruriens is the best. It

contains, L dopa, so converts straight to dopamine really easily, and

you won't have to take laods of additinal things to convert it. Most

people seem to find this quite strong. It crosses the blood brain

barrier more easily than some other suppliments. I am going to try to

get hold of some ASAP.

Smoking actually lowers NO, and damages neurons. I think I will try

to quit after the exams. Eating dark chocolate is better, it raises

lots of chemicals that you need, eg. NO, norepherephine, adrenaline.

February 18, 2008

In that case, you can just take cialis and stop taking any other

suppliment. Cialis and viagra upgrade No.

If your theory is correct, then ther is nothing else you need to worry

about?

February 19, 2008

well cant a lot of people on here get an erection while they are on

these kind of drugs?

all those drugs do not effect nitric oxide *synthesis* they contain

nitric oxide and they inhibit the enzyme witch breaks it down.

those drugs are just a band aid not a cure.

>

> In that case, you can just take cialis and stop taking any other

> suppliment. Cialis and viagra upgrade No.

>

> If your theory is correct, then ther is nothing else you need to

worry

> about?

>

February 20, 2008

Hm, yes that's true.

I do think you are right in some respects. People with pssd probably

have some kind of problem with nitric oxide (I have said that all

allong).

However, i don't think those drugs really work amazingly well. The

first stage oif erection is not working very well either -

the " sympathetic muscular impulses " as they are called. I think this is

caused by desensitized dopamine/ muscarinic / adrenaline /

neuropherephine systems. As I have said before there is a hormone that

resensitizes these systems (the hormone involved in sleep deprivation

recovery and hunger pangs and running exercises).

April 19, 2009

go easy on dosage, or try different dosage. I personally had better sucess with

low tyrosine dosage over high. its wierd but body seems to react very

differently. I was able to reverse some pssd symptoms trying low dosage tyrosine

but not while trying high dose.

> >

> > I think you're missing the point. A lot of doctors say that " nitric

> > oxide is the key to erections " or something like that.

> >

> > Actually there are many chemicals involved - dopamine, serotonin,

> > gaba, oxytopin, histamines, testosterone, acetylcholine,

> > norepherephine, and adrenaline of course.

> >

> > I think nitric oxide IS definetely a problem in pssd. However, the

> > thing about niric oxide is that it isn't nitric oxide that causes

> > erections really. Nitric oxide just causes the blood vessles to

> > relax, making it easier to get an erection.

> >

> > I have tried things like amyl nitrate and levitra, and I'm sure you

> > have tried cialis etc. These chemicals make it easier to maintain an

> > erection. However, they do not really work. From what I have been

> > reading recetly, cialis etc, directly signal nitric oxide to enter

> > the penis. This helps to enhance erectiosn, but that's about it.

> >

> > I think you make too much of the connection with serotonin. There are

> > lots of things that influence nitric oxide, and the main things are

> > histamines, l-argine etc. The idea that people with high serotonin

> > have low NO, and vice cersa is too simplistic. For instance, you told

> > me that eating chocolate would lower NO levels because it raises

> > serotonin. It probably does raise serotonin, but if you look around

> > you'll see that it also raises NO levels, so much so that some people

> > eat it for heart disease!

> >

> > PSSD probably causes a number of chemical imbalances. The hardest

> > one's to correct are where certain transmittors are not " signalling "

> > properly I believe. I think this could be a problem with genes,

> > proteins, enzymes etc.

> >

> > However, MDMA did work for me. I think this shows that people with

> > PSSD could get better with the right chemicals.

> >

> > I feel like I have a good understanding of how arousal works now.

> >

> > You need a good amount of chemicals that give you the more " orgasmic "

> > sort of feelings and get rid of the numbeness etc. I think this

> > propbably includes GABA, dopamine, norepherephine, oxytopin and

> > possibly acetylcholine.

> >

> > I think what actually causes the reection to take place is increased

> > blood flow to the penis. This is caused by excitement. Sexual

> > excitement is caused mainly by things like dopamine, oxytopin and

> > norepherephine I think. Adrenaline causes blood flow to increase.

> > Also I have noticed that acetylcholine probably helps you to ralax,

> > thus helping at this stage.

> >

> > And of course, your blood vessels need to relaxe, thus causing the

> > blood to enter, and stay in etc. This is a rush of nitric oxide,

> > aminly caused by dopamine etc. It is possible that other things are

> > involved such as acetylcholine involved.

> >

> > I think where you need to start, is by improving your dopamine

> > suppliments. Vitamin B and fish oils is ok, but really not a very

> > strong intake. At the moment I am taking l-phenalenaline, vit B6,

> > magnesium, zinc, vitamin C, niacin, and folic acids. All of those are

> > needed to convert dopamine. However, dopamine is really difficult to

> > convert. Most people have found that Mucuna Pruriens is the best. It

> > contains, L dopa, so converts straight to dopamine really easily, and

> > you won't have to take laods of additinal things to convert it. Most

> > people seem to find this quite strong. It crosses the blood brain

> > barrier more easily than some other suppliments. I am going to try to

> > get hold of some ASAP.

> >

> > Smoking actually lowers NO, and damages neurons. I think I will try

> > to quit after the exams. Eating dark chocolate is better, it raises

> > lots of chemicals that you need, eg. NO, norepherephine, adrenaline.

> >

>

April 19, 2009

i will be intersted to hear your results with the muriens. i think i took it a while ago - cant remember i've tried so much - but all i can recall is that i started to see visual images when i shut my eyes, that never had happened to me before and i dont think it helped the libido at all. thyrosine does help and i agree that less is more.To:

SSRIsex Sent: Sunday, April 19, 2009 12:34:15 PMSubject: Re: down regulation of nitric oxide

Sign In

down regulation of nitric oxide

Recommended Posts

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Join the conversation

Activity