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Characterization of endothelin receptors in rat renal artery in vitro
Author(s) -
Clark Kenneth L.,
Pierre Lisa
Publication year - 1995
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 - 10.1111/j.1476-5381.1995.tb13273.x
Subject(s) - endothelin receptor , receptor , medicine , endocrinology , agonist , antagonist , contraction (grammar) , receptor antagonist , endothelins , chemistry , thromboxane a2 , thromboxane , biology , platelet
1 The aim of this study was to investigate the function and characteristics of endothelin receptors in rat main branch renal artery in vitro . 2 Endothelin(ET)‐1 (mean EC 50 = 9.8 n m ) was approximately 12 fold more potent than ET‐3 (mean EC 50 = 120 n m ) as a contractile agonist and produced a greater maximum response. In contrast, neither of the ET B receptor‐selective agonists, alanine 1,13,11,15] ET‐1 nor sarafotoxin S6c, (0.1 n m ‐1 μ m ), induced any contractile effect, or any relaxant effect in endothelium‐intact preparations pre‐contracted with the thromboxane A 2 mimetic, U‐46619. Sarafotoxin S6c (30 n m ) also failed to induce any further contraction in tissues pre‐contracted with an EC 50 concentration of ET‐1. 3 The ET A receptor‐selective antagonist, BQ123, behaved as a weak and variable antagonist of the contractile effects of ET‐1 (mean pA 2 estimates in the range 5.8–6.3). In contrast, BQ123 antagonized ET‐3 with a potency (mean pA 2 = 7.6) consistent with its affinity for ET A receptors. Co‐incubation of BQ123 (3 μ m ) with the putative ET B receptor‐selective antagonist, IRL1038 (10 μ m ), produced no greater antagonism of ET‐1 responses than was induced by BQ123 (3 μ m ) alone. 4 In conclusion, ET B receptors do not appear to be present in rat main branch renal artery. The contractile effects of ET‐3 in this tissue seem to be mediated by ET A receptors. While ET A receptors partly mediate the contractile effects of ET‐1, these data raise the possibility that a population of novel BQ123‐insensitive endothelin receptors may also contribute to this response.