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Effect of Endothelin-1 on Corticosteroid Secretion by the Frog Adrenal Gland Is Mediated by an Endothelin_A Receptor¹

European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, Institut National de la Santé et de la Recherche Médicale (INSERM U413), Unité Affiliée au Centre National de la Recherche Scientifique (UA CNRS), University of Rouen (F.C., I.R.J., H.V., C.D.), 76821 Mont-Saint-Aignan, France; and Institut National de la Recherche Scientifique-Santé (INRS-Santé), University of Québec (A.F.), Pointe-Claire, Québec, Canada H9R 1G6

Address all correspondence and requests for reprints to: Hubert Vaudry, European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U413, UA CNRS, University of Rouen, 76821 Mont-Saint-Aignan, France. E-mail: hubert.vaudry{at}univ-rouen.fr

We have previously reported that endothelin-1 (ET-1) stimulates the in vitro secretion of corticosterone and aldosterone from the adrenal gland of the frog Rana ridibunda. The aim of the present study was to investigate the pharmacological profile of the endothelin receptor subtype involved in the corticotropic effect of ET-1. The mixed ET_A/ET_B receptor antagonist Ro 47–0203 (10^-5 M) totally blocked the stimulatory effect of ET-1 (5 x 10^-9 M) on corticosterone and aldosterone secretion. The action of ET-1 was also inhibited by the selective ET_A receptor antagonist BQ-485 (10^-7 M). In contrast, the selective ET_B receptor antagonist IRL 1038 (10^-6 M) did not affect the response of the frog adrenal gland to ET-1. In addition, the selective ET_B receptor agonist IRL 1620 (10^-6 M) did not mimic the stimulatory effect of ET-1. The high affinity ET_C receptor agonist endothelin-3 (ET-3) stimulated corticosteroid secretion, but was 400 times less potent than ET-1. Moreover, the action of ET-3 was also blocked by BQ-485 (10^-7 M). These data indicate that the stimulatory effects of ET-1 and ET-3 on corticosteroid secretion by the frog adrenal gland are mediated by an ET_A receptor subtype.

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