Hypoxic coronary vasodilatation and cGMP overproduction are blocked by a nitric oxide synthase inhibitor, but not by a guanylyl cyclase ANF receptor antagonist. Academic Article uri icon

Overview

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 date

  • April 11, 1994

Research

keywords

  • Amino Acid Oxidoreductases
  • Atrial Natriuretic Factor
  • Coronary Circulation
  • Cyclic GMP
  • Guanylate Cyclase
  • Hypoxia
  • Receptors, Atrial Natriuretic Factor
  • Vasodilation

Identity

Scopus Document Identifier

  • 0028224027

Digital Object Identifier (DOI)

  • 10.1016/0014-2999(94)90622-x

PubMed ID

  • 7517893

Additional Document Info

volume

  • 256

issue

  • 1