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Endothelin-1 induces vasoconstriction and nitric oxide release via endothelin ETBreceptors in isolated perfused rat liver

European Journal of Pharmacology
Publication Date
DOI: 10.1016/s0014-2999(97)83043-9
  • Endothelin
  • Endothelin Etareceptor
  • Endothelin Etbreceptor
  • Pressor Effect
  • Nitric Oxide (No)
  • Oxygen Consumption
  • Liver


Abstract Endothelin-1 (0.1, 1 and 10 nM) induced a significant increase in portal pressure and nitric oxide (NO) release in the isolated rat liver. The endothelin ET B receptor agonist, IRL 1620 (Suc-[Glu 9,Ala 11,15]endothelin-1-(8–21)) (0.1, 1 and 10 nM) also elicited a marked increase in portal pressure and NO release. The potency of endothelin-1 was higher than that of IRL 1620. The endothelin ET A receptor antagonist, BQ-123 ( cyclo(- d-Trp- d-Asp-Pro- d-Val-Leu)) (1 and 10 μM), had no effect on the endothelin-1-induced change in portal pressure and NO current. In contrast, the endothelin ET B receptor antagonist, BQ-788 ( N- cis-2,6-dimethylpiperidinocarbonyl- l-γ-methylleucyl- d-1-methoxycarbonyltryptophanyl- d-norleucine) (1 and 10 nM), attenuated the endothelin-1-induced change in portal pressure and NO current. Administration of N G-monomethyl- l-arginine ( l-NMMA), a NO synthase inhibitor, completely abolished the endothelin-1- or IRL 1620-induced NO release. l-NMMA enhanced the increase in portal pressure and decrease in O 2 consumption caused by endothelin-1. These results indicated that endothelin ET B receptors mediate both vasoconstriction and NO release and that NO plays a significant role in stabilizing microcirculation in isolated perfused rat liver.

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