Abstract
Studies using an inhibitor of nitric oxide (NO) synthesis have suggested that endogenous NO may have a role in regulating endothelin release. We investigated the effect of endogenous and exogenous nitric oxide (NO) on the release of irET-1. L-NAME stimulated, but L-arginine inhibited irET-1 release. Perfusing sodium nitroprusside (SNP), however, did not inhibit irET-1 secretion. CyclicGMP, the second messenger for NO action, was stimulated by SNP but not by L-arginine. These data demonstrate that endogenous NO inhibits of irET-1, in a manner which is independent of cGMP, and suggest that this action may contribute to the vasodilatory effect of NO.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenal Glands / drug effects*
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Adrenal Glands / metabolism*
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Adrenal Glands / physiology
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Animals
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Arginine / analogs & derivatives
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Arginine / pharmacology
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Cyclic GMP / biosynthesis
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Endothelins / metabolism*
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Enzyme Inhibitors / pharmacology
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In Vitro Techniques
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Male
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NG-Nitroarginine Methyl Ester
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Nitric Oxide / pharmacology*
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Nitric Oxide / physiology*
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitroprusside / pharmacology
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Perfusion
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Rats
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Rats, Wistar
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Second Messenger Systems / drug effects
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Second Messenger Systems / physiology
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Vasodilation / physiology
Substances
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Endothelins
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Enzyme Inhibitors
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Nitroprusside
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Nitric Oxide
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Arginine
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Nitric Oxide Synthase
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Cyclic GMP
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NG-Nitroarginine Methyl Ester