Abstract
Nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) represent the two major endothelial autacoids involved in the local control of vascular tone. Here we describe a novel pathway leading to the calcium-independent activation of the endothelial NO synthase by shear stress and enhanced cellular tyrosine phosphorylation. In addition we present evidence that NO inhibits the formation of EDHF, which we have characterized as a transferable, beta-naphthoflavone-inducible P450-dependent metabolite of arachidonic acid.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aorta / enzymology
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Aorta / metabolism
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Biological Factors / biosynthesis*
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Biological Factors / metabolism
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Bradykinin / pharmacology
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Calcium / metabolism*
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Calcium / pharmacology
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Coronary Vessels / drug effects
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Coronary Vessels / enzymology*
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Coronary Vessels / metabolism
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Cytochrome P-450 Enzyme System / metabolism
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Dose-Response Relationship, Drug
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Hemorheology
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / enzymology
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Muscle, Smooth, Vascular / metabolism
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Nitric Oxide / biosynthesis*
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Nitric Oxide / metabolism
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Nitric Oxide Synthase / metabolism
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Phospholipases A / metabolism
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Phosphorylation
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Rabbits
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Rats
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Swine
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Tyrosine / chemistry
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Vasodilation / drug effects
Substances
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Biological Factors
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endothelium-dependent hyperpolarization factor
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Nitric Oxide
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Tyrosine
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Cytochrome P-450 Enzyme System
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Nitric Oxide Synthase
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Phospholipases A
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Bradykinin
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Calcium