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Pharmacological characterization of endothelin‐induced rat pulmonary arterial dilatation
Author(s) -
Higashi Tooru,
Ishizaki Takeshi,
Shigemori Kazuo,
Yamamura Takaki,
Nakai Tuguhiko
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701177
Subject(s) - endothelin receptor , medicine , endothelins , endothelin 1 , cardiology , pharmacology , receptor
The aim of study was to characterize endothelin (ET)‐induced vasodilatation in isolated extrapulmonary rat arteries (EPA) and in intrapulmonary arteries (IPA) preconstricted with 1 μ M phenylephrine. The ET‐3 (1 n M –100 n M )‐ and ET‐1 (10 n M –100 n M )‐induced transient vasodilatations in EPA were more potent than those in IPA. The vasodilatation induced by ET‐3 (100 n M ) was larger than that induced by ET‐1 (100 n M ). Both the ET B antagonist, BQ788 (3 μ M ) and or endothelium denudation, but not the ET A antagonist, BQ123 (3 μ M ), abolished the vasodilatation induced by ET‐1 or ET‐3 (100 n M each) in EPA and in IPA. The ATP‐sensitive K+channel blocker, glibenclamide (20 μ M ) and the nitric oxide synthase inhibitor, N G ‐monomethyl‐ L ‐arginine ( L ‐NMMA, 1 m M ) suppressed the ET‐induced vasodilatation in EPA and in IPA. We conclude that the vasodilatation induced by endothelins is markedly reduced in rat isolated IPA, and suggest that the endothelial ET B ‐mediated vasodilatation varies depending on rat pulmonary arterial regions. Furthermore, ET B ‐mediated vasodilatation involves activation of ATP‐sensitive K + channels and of nitric oxide synthase in rat isolated EPA and IPA.British Journal of Pharmacology (1997) 121 , 782–786; doi: 10.1038/sj.bjp.0701177