Abstract
Nitric oxide (NO) derived from the endothelial NO synthase (eNOS) has antihypertensive, antithrombotic, anti-atherosclerotic and antiobesogenic properties. Resveratrol is a polyphenol phytoalexin with multiple cardiovascular and metabolic effects. Part of the beneficial effects of resveratrol are mediated by eNOS. Resveratrol stimulates NO production from eNOS by a number of mechanisms, including upregulation of eNOS expression, stimulation of eNOS enzymatic activity and reversal of eNOS uncoupling. In addition, by reducing oxidative stress, resveratrol prevents oxidative NO inactivation by superoxide thereby enhancing NO bioavailability. Molecular pathways underlying these effects of resveratrol involve SIRT1, AMPK, Nrf2 and estrogen receptors.
Highlights
Endothelial Nitric OxideNitric oxide (NO) is produced by three isoforms of NO synthase (NOS): the neuronal nNOS (NOS I), the inducible iNOS (NOS II) and the endothelial endothelial NO synthase (eNOS) (NOS III)
Nitric oxide (NO) derived from the endothelial NO synthase has antihypertensive, antithrombotic, anti-atherosclerotic and antiobesogenic properties
sirtuin 1 (SIRT1) [56,57] and endothelial NO synthase (eNOS) [58] have been implicated in the effect of resveratrol on endothelial progenitor cell (EPC)
Summary
Nitric oxide (NO) is produced by three isoforms of NO synthase (NOS): the neuronal nNOS (NOS I), the inducible iNOS (NOS II) and the endothelial eNOS (NOS III). Vascular NO is mainly produced by eNOS This enzyme is constitutively expressed in the endothelium and is activated by shear stress or by agonists such as bradykinin and acetylcholine. Endothelial NO relaxes blood vessels and reduces blood pressure. It diffuses from endothelial cells into the underlying smooth muscle cells and induces vasodilation by stimulating NO-sensitive guanylyl cyclase. NO produced by the endothelial eNOS diffuses into the blood and inhibits platelet aggregation and adhesion. In addition to these antihypertensive and antithrombotic actions, eNOS-derived. Overexpression of eNOS prevents weight gain in high fat-fed mice by stimulating mitochondrial biogenesis and activity in adipose tissues [9]
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