Nitric Oxide Supplements

from Wikipedia said:

Nitric oxide is an air pollutant produced by combustion of substances in air, like in automobile engines

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db1 said:

It's therfore marketed mainly as a body building suppliment (whixh is what I intend to use it for) but it is also thought to help with the damage that highblood sugars can cause to the cardiovascular and nervous system, studies have shown..

So it'd be great if anyone that has had experience with NO suppliments, or body building could recomend any.

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Curr Drug Targets Cardiovasc Haematol Disord. 2004 Mar;4(1):1-11.
Molecular mechanisms of impaired endothelial function associated with insulin resistance.
Shinozaki K, Kashiwagi A, Masada M, Okamura T.
Source

Department of Pharmacology, Shiga University of Medical Science, Otsu, Japan.
Abstract

Dysfunction of the endothelium in large- and medium-sized arteries plays a central role in atherogenesis. The insulin resistance syndrome encompasses more than a subnormal response to insulin-mediated glucose disposal. Patients with this syndrome also frequently display elevated blood pressure, hyperlipidemia, and dysfibinolysis, even without any clinically manifested alteration in plasma glucose concentrations. Of note endothelial dysfunction and atherosclerosis also have been demonstrated in patients with hypertension, which is one of the features of the syndrome of insulin resistance. Insulin-induced vasodilation, which is mediated by the release of nitric oxide (NO) release, is impaired in obese individuals who display insulin resistance. Although it is tempting to speculate that loss of endothelium-dependent vasodilation and increased vasoconstriction might be etiological factors of elevated blood pressure, the factors contributing to NO-mediated endothelial dysfunction in the insulin-resistant state are not fully defined. Experimental evidences suggest that (6R)-5,6,7,8-tetrahydrobiopterin (BH(4)), the natural and essential cofactor of NO synthases (NOS), plays a crucial role not only in increasing the rate of NO generation by NOS but also in controlling the formation of superoxide anion (O(2)(-)) in the endothelial cells. Under insulin-resistant conditions where BH(4) levels are suboptimal, in addition to a reduced synthesis of NO, an accelerated inactivation of NO by O(2)(-) within the vascular wall was observed. Furthermore, oral supplementation of BH(4) restored endothelial function and relieved oxidative tissue damage, through activation of eNOS in the aorta of insulin-resistant rats. These results indicate that abnormal pteridine metabolism contributes to causing endothelial dysfunction and the enhancement of vascular oxidative stress in the insulin-resistant state.

PMID:
15032648
[PubMed - indexed for MEDLINE]

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Biofactors. 2009 Jan-Feb;35(1):21-7.
Nitric oxide and vascular insulin resistance.
Wu G, Meininger CJ.
Source

Department of Animal Science and Faculty of Nutrition, Texas A&M University, College Station, TX 77843-2471, USA. g-wu@tamu.edu
Abstract

Obesity and type-II diabetes are growing major health issues worldwide. They are the leading risk factors for vascular insulin resistance, which plays an important role in the pathogenesis of cardiovascular disease, the leading cause of death in developed nations. Recent studies have shown that reduced synthesis of nitric oxide (NO; a major vasodilator) from L-arginine in endothelial cells is a major factor contributing to the impaired action of insulin in the vasculature of obese and diabetic subjects. The decreased NO generation results from a deficiency of (6R)-5,6,7,8-tetrahydrobiopterin [BH4; an essential cofactor for NO synthase (NOS)], as well as increased generation of glucosamine (an inhibitor of the pentose cycle for the production of NADPH, another cofactor for NOS) from glucose and L-glutamine. Accordingly, endothelial dysfunction can be prevented by (1) enhancement of BH4 synthesis through supplementation of its precursor (sepiapterin) via the salvage pathway; (2) transfer of the gene for GTP cyclohydrolase-I (the first and key regulatory enzyme for de novo synthesis of BH4); or (3) dietary supplementation of L-arginine (which stimulates GTP cyclohydrolase-I expression and inhibits hexosamine production). Modulation of the arginine-NO pathway by BH4 and arginine is beneficial for ameliorating vascular insulin resistance in obesity and diabetes.

(c) 2009 International Union of Biochemistry and Molecular Biology, Inc.

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