cyclosporine in stachybotrys and hypertension

[Guest guest]

The cyclosporin in stachybotrys may be responsible for some of its

permanent effects just as cyclosporin has many negative, permanent

side effects when it is used to suppress the immune system in

medicine.

For example, I typed in cyclosporine and hypertension and I got back

thousands of hits. Here are two from the first 20 results.

Pathophysiology. 2007 Oct 17; [Epub ahead of print]

Mitochondrial energy conversion disturbance with decrease in ATP

production as a source of systemic arterial hypertension.

Postnov YV, Orlov SN, Budnikov YY, Doroschuk AD, Postnov AY.

Russian Cardiology Research and Production Complex, Moscow, Russia.

Despite numerous efforts, including recent genetic and molecular

biology studies, the immediate cause of stationary elevated blood

pressure (BP) in any kind of hypertension has not been satisfactorily

explained. This review deals with the cellular mechanisms underlying

decreased energy status documented in different tissues from

experimental rat models of primary and secondary hypertension as well

as the involvement of these abnormalities in the pathogenesis of the

disease. Such analyses allow us to hypothesize that dysfunction of

mitochondrial energy conversion, caused by distinct stimuli, including

generalized disturbances of intracellular Ca(2+) handling and

mitochondria calcium overload found in primary hypertension, leads to

uncoupling of oxidation and phosphorylation and attenuated ATP

synthesis. Examples of arterial hypertension accompanied by

mitochondrial uncoupling and cell ATP depletion (hyperthyroidism, cold

hypertension, cyclosporine A intake, etc.) may be considered as an

additional argument supporting this opinion. It means also that

despite of differences in triggering mechanisms of mitochondrial

dysfunction in all these models, the final outcome, i.e. decreased

mitochondrial ATP production, is similar. Attenuated intracellular ATP

content, in turn, results in the long-term maintenance of elevated BP

by increased sympathetic outflow, whereas augmented ROS production

following mitochondrial dysfunction lowers the capacity of the

NO-dependent vascular relaxation. In the light of these data the cause

of stationary elevated BP in chronic arterial hypertension should be

regarded as a compensatory response to decreased mitochondrial ATP

synthesis.

PMID: 17949954 [PubMed - as supplied by publisher]

Urol J. 2004 Winter;1(1):19-23.

The Newest Medications in Kidney Transplantation and their Mechanisms of Action.

Lessan-Pezeshki M.

Division of Nephrology, Imam Khomeini Hospital, Tehran University of

Medical Sciences, Tehran, Iran.

Introduction: In recent years, many new immunosuppressive drugs have

been discovered and developed for clinical use in transplantation.

This review focuses on new drugs and novel strategies that have been

shown to have immunosuppressive activity in patients. Materials and

Methods: The literature was reviewed. Results: The introduction of

cyclosporine in the early 1980s improved renal allograft survival by

approximately 15 percent at one year post transplant. However,

cyclosporine failed to enhance long term graft survival. In addition,

transplant recipients are at risk of significant side effects due to

immunosuppression, including infection, cardiovascular disease,

hypertension and malignancy. The limitations constitute the rational

for the continued development of new immunosuppressive agents.

Conclusion: The therapeutic armamentarium for transplant

immunosuppression continues to broaden and become more complex, as

does the variety of potential drug combinations or protocols. Further

studies in a large number of individuals are required to clarify the

role of new immunosuppressive agents and novel strategies in

transplant recipients.

PMID: 17874406 [PubMed - in process]