Posted by raybakes on October 29, 2004, at 7:12:25
In reply to Re: Help needed with cholinergic drug reactions? » raybakes, posted by tealady on October 27, 2004, at 22:34:20
Hi Jan, good luck with your studying - just came across this abstract that seemed to tie in a lot of the things you are talking about. Superoxide excess seems to be a common thread in inhibiting the vasodilation and sodium balance in the kidney. Nitric oxide turns from a vasodilator to a vasoconstrictor when it combines with superoxide to form peroxynitrite - you didn't say what you had at the dentist, but if it was nitrous oxide, it might have been able to form peroxynitrite too - nitrites in bacon can definitely produce peroxynitrite.
Just found out that sulfites can trigger NADPH oxidase, and produce superoxide - seems to fit the pattern quite well! NADPH is needed for glutathione formation (nitric oxide, dopa, serotonin, steroid hormone synthesis, noradrenaline and folate activation!), so to lose too much is disasterous.
If you think this relates to you, arginine might be beneficial, but healing the endothelium cells to allow proper vasodilation to occur (not forgetting dealing with superoxide). I've used Venocap by Thorne research to help my endothelial cells - it contains, witch hazel, horse chestnut, butchers broom, gotu cola, grape seed extract. Lar gave me a link to an article by Dr Pall on peroxynitrite on a recent thread.
Nitric oxide, oxidative stress, and progression of chronic renal failure.
Modlinger PS, Wilcox CS, Aslam S.
Division of Nephrology and Hypertension, Georgetown University Medical Center, Washington, DC 20007, USA.
Cellular injury or organ dysfunction from oxidative stress occurs when reactive oxygen species (ROS) accumulate in excess of the host defense mechanisms. The deleterious effect of ROS occurs from 2 principal actions. First, ROS can inactivate mitochondrial enzymes, damage DNA, or lead to apoptosis or cellular hypertrophy. Second, nitric oxide (NO), which is a principal endothelial-derived relaxing factor, reacts with superoxide anion (O2-) to yield peroxynitrite (ONOO-), which is a powerful oxidant and nitrosating agent. The inactivation of NO by O2- creates NO deficiency. Oxidative stress can promote the production of vasoconstrictor molecules and primary salt retention by the kidney. Several hypertensive animal models showed increased activity of nicotine adenine dinucleotide phosphate (NADPH) oxidase, which is the chief source of O2- in the vessel wall and kidneys. NO regulates renal blood flow, tubuloglomerular feedback (TGF), and pressure natriuresis. Animal models of NO deficiency develop hypertension, proteinuria, and glomerulosclerosis. Evidence is presented that chronic renal failure (CRF) is a state of NO deficiency secondary to decreased kidney NO production and/or increased bioinactivation of NO by O2-. Patients with CRF show decreased endothelium-dependent vasodilatation to acetylcholine, have increased markers of oxidative stress, and diminished antioxidant activity. Therapy for oxidative stress has focused on antioxidants and agents that modify the renin-angiotensin system. The effects of such treatments are more compelling in animal models than in human studies.
poster:raybakes
thread:359642
URL: http://www.dr-bob.org/babble/alter/20041022/msgs/408679.html