Endothelin-3 stimulates production of endothelium-derived nitric oxide via phosphoinositide breakdown

Biochem Biophys Res Commun. 1991 Jan 15;174(1):228-35. doi: 10.1016/0006-291x(91)90510-e.

Abstract

Cultured bovine endothelial cells (EC) have specific receptors for endothelin (ET)-3 functionally coupled to phosphoinositide breakdown. We studied whether ET-3 stimulates synthesis of nitric oxide (NO), an endothelium-derived relaxing factor that activates soluble guanylate cyclase in EC, and whether the ET-3-induced NO formation involves G-proteins. ET-3 dose-dependently stimulated production of intracellular cGMP in EC, of which effects were abolished by pretreatment with NG-monomethyl L-arginine, an inhibitor of NO synthesis, and methylene blue, an inhibitor of soluble guanylate cyclase. The stimulatory effects of ET-3 on cGMP production, inositol trisphosphate formation and increase in cytosolic free Ca2+ concentration were similarly blocked by pretreatment with pertussis toxin (PTX). These data suggest that ET-3 induces synthesis of NO mediated by phosphoinositide breakdown via PTX-sensitive G-protein in EC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism
  • Cattle
  • Cells, Cultured
  • Cyclic GMP / metabolism
  • Dose-Response Relationship, Drug
  • Endothelins / administration & dosage
  • Endothelins / pharmacology*
  • GTP-Binding Proteins / metabolism
  • Inositol 1,4,5-Trisphosphate / metabolism
  • Nitric Oxide / metabolism*
  • Pertussis Toxin
  • Phosphatidylinositols / metabolism*
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Endothelins
  • Phosphatidylinositols
  • Virulence Factors, Bordetella
  • Nitric Oxide
  • Inositol 1,4,5-Trisphosphate
  • Pertussis Toxin
  • GTP-Binding Proteins
  • Cyclic GMP
  • Calcium