Ann Vasc Dis. 2018 Mar 25;11(1):41-51.
Nitric Oxide: From Good to Bad.Vanhoutte PM1.
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AbstractThis essay summarizes a lecture presented on October 19th, 2017, during the 58th Annual Meeting of the Japanese College of Angiology in Nagoya, Japan. The lecture summarizes several instances where the absence of relaxations of isolated blood vessels in response to endothelium-dependent vasodilator agonists, which cause activation of endothelial nitric oxide synthase (eNOS) and consequent production of endothelium-derived nitric oxide (NO) and stimulation of soluble guanylyl cyclase (sGC) in underlying vascular smooth muscle, or hypoxia are curtailed or reversed to endothelium-dependent contractions. Chosen examples include selective dysfunction of eNOS activation in regenerated endothelial cells, unresponsiveness of vascular smooth muscle cells to NO during subarachnoid hemorrhage, and biased activation of sGC in vascular smooth muscle cells during acute exposure to hypoxia. KEYWORDS:endothelial nitric oxide synthase; endothelium; nitric oxide; soluble guanylyl cyclase; vascular smooth muscle |
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