This proven impairment in NOS (Nitric Oxide Synthases) production is related to aging and is also proven to occur with low level lead accumulation and responds to Chelation. This is why I teach in all my lectures now for years that oral or IV Chelation does not need to reverse plaque since it is documented to improve blood flow. It is because we all have low level lead accumulation so this so called "aging change" is not just aging but is directly related to the low level lead toxicity we all suffer today. Unless you stay on oral chelation without fail for at least 15 years your bones will always have highly concentrated stores of lead to interfere with Nitric Oxide synthases so you are not converting Arginine to NO efficiently unless you routinely chelate to lower available lead levels in your body.
Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
http://www.gordonresearch.com Effect of aging on nitric oxide synthase signaling in coronary arterioles:
Role of phosphotidylinositol 3-kinase
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http://web.nerac.com/access/WPRNDN1A?NDN=24404011595&C=09045500 AUTHORS- LeBlanc, Amanda Jo; Shipley, Robert D.; Muller-Delp, Judy
JOURNAL NAME- FASEB Journal VOLUME 20 NUMBER 5, Part 2 PUBLICATION DATE- 2006, MAR 7 2006 PP A1397 DOCUMENT TYPE- Meeting ISSN-0892-6638 ADDRESS- W Virginia Univ, Ctr Interdisciplinary Res Cardiovasc Sci, Morgantown, WV 26506 USA SPONSOR- Amer Assoc Anatomists; Amer Physiol Soc; Amer Soc Biochem & Mol Biol; Amer Soc Investigat Pathol; Amer Soc Nutr; Amer Soc Pharmacol & Expt Therapeut CONFERENCE DATE- April 01 -05, 2006 CONFERENCE TITLE- Experimental Biology 2006 Meeting
Flow-dependent vasodilation is impaired in coronary arterioles from aged rats; however, acetylcholine (ACh)-induced vasodilation is preserved with age. Both of these vasodilatory responses are mediated entirely though the production of nitric oxide (NO). Recent data indicate that basal NO production is significantly reduced in arterioles from old versus young rats (p=0.001), but ACh-stimulated NO production remains intact in arterioles from old rats. Therefore, we sought to determine whether the >age-related< decrease in flow-induced vasodilation is due to the impairment of upstream signaling mechanisms that mediate the release of NO. Specifically, we tested the hypothesis that phosphotidylinositol 3-kinase (PI3-kinase)-mediated release of NO is decreased in coronary arterioles from aged rats compared to young rats. Coronary arterioles were isolated from young (4 mos) and old (24 mos) male Fischer-344 rats to assess flow- and VEGF-induced vasodilation. Both flow- and VEGF-induced vasodilation of coronary arterioles were impaired with age. Wortmannin, an inhibitor of PI3-kinase, abolished >age-related< differences in flow-induced vasodilation (p=0.58). These data suggest that PI3-kinase-mediated activation of nitric oxide synthase (NOS) in coronary arterioles is impaired with advancing age.
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