Endothelin-1 induces vasoconstriction through two functionally distinct pathways in porcine coronary artery: Contribution of phosphoinositide turnover

Yoshitoshi Kasuya, Yoh Takuwa, Masashi Yanagisawa, Sadao Kimura, Katsutoshi Goto, Tomoh Masaki

Research output: Contribution to journalArticle

96 Scopus citations

Abstract

Endothelin-1 (ET1)-induced contraction of isolated porcine coronary artery strips was previously reported to be mainly dependent on extracellular Ca2+. However, even in a Ca2+-free, EGTA-containing solution relatively high concentrations of ET1 induced a weak vasoconstriction, which was markedly but not completely inhibited by pretreatment with caffeine. Over similar dose ranges, ET1 stimulated the production of inositol phosphates in a dose-dependent manner in intact arterial tissues, which was independent of extracellular Ca2+ and was not affected by receptor blockers such as atropine, methysergide and diphenhydramine. Moreover, ET1 was shown to induce an increase in 1,2-diacylglycerol. These results indicate that the activation of ET1 receptors on porcine coronary artery smooth muscle causes phosphoinositide breakdown, leading to intracellular Ca2+ mobilization and protein kinase C activation. It is suggested that phospholipase C-mediated phosphoinositide breakdown as well as previously reported activation of voltage-dependent Ca2+ channels are involved in the mechanism of ET1-induced vasoconstriction.

Original languageEnglish (US)
Pages (from-to)1049-1055
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume161
Issue number3
DOIs
StatePublished - Jun 30 1989

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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