Abstract
Myocardial hypoxia is known to be accompanied by the release of atrial natriuretic factor (ANF), a peptide which dilates the coronary vessels by stimulating particulate guanylyl cyclase. We have assessed whether ANF plays a paracrine role in hypoxic coronary vasodilatation, a reaction which we had previously found to be associated with increased cyclic GMP production. Compound HS 142-1 (100 micrograms/ml), a specific antagonist of the guanylyl cyclase ANF receptor, inhibited by 50-70% the coronary-vasodilating effects of human ANF (1-10 micrograms) administered to isolated guinea pig hearts, but affected neither hypoxic coronary vasodilation nor cyclic GMP overflow. In contrast, the nitric oxide synthase inhibitor N omega-methyl-L-arginine (300 microM) reduced hypoxic coronary vasodilatation and cyclic GMP overproduction by approximately 70% and 50-60%, respectively. Thus, unlike nitric oxide, ANF appears not to play a paracrine role in hypoxic coronary vasodilatation.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Oxidoreductases / antagonists & inhibitors*
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Animals
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Arginine / analogs & derivatives
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Arginine / pharmacology
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Atrial Natriuretic Factor / antagonists & inhibitors*
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Coronary Circulation / drug effects
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Coronary Circulation / physiology*
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Cyclic GMP / biosynthesis*
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Guanylate Cyclase / antagonists & inhibitors*
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Guinea Pigs
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Humans
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Hypoxia / metabolism
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Hypoxia / physiopathology*
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In Vitro Techniques
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Male
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Nitric Oxide / antagonists & inhibitors
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Nitric Oxide Synthase
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Perfusion
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Polysaccharides / pharmacology
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Receptors, Atrial Natriuretic Factor / antagonists & inhibitors*
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Receptors, Atrial Natriuretic Factor / drug effects
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Vasodilation / drug effects
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Vasodilation / physiology*
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omega-N-Methylarginine
Substances
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HS 142-1
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Polysaccharides
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omega-N-Methylarginine
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Nitric Oxide
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Atrial Natriuretic Factor
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Arginine
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Nitric Oxide Synthase
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Amino Acid Oxidoreductases
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Guanylate Cyclase
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Receptors, Atrial Natriuretic Factor
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Cyclic GMP