Evidence for a new angiotensin-(1-7) receptor subtype in the aorta of Sprague-Dawley rats.
Silva, D. M.R. a,1; Vianna, H. R. a,1; Cortes, S. F. b; Campagnole-Santos, M. J. a; Santos, R. A.S. a; Lemos, V. S. a,*
[Article]
Peptides.
28(3):702-707, March 2007.
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: We have recently described, in the mouse aorta, the vasodilator effect of angiotensin-(1-7) (Ang-(1-7)) was mediated by activation of the Mas Ang-(1-7) receptor and that A-779 and D-Pro7-Ang-(1-7) act as Mas receptor antagonists. In this work we show pharmacological evidence for the existence of a different Ang-(1-7) receptor subtype mediating the vasodilator effect of Ang-(1-7) in the aorta from Sprague-Dawley (SD) rats. Ang-(1-7) induced an endothelium-dependent vasodilator effect in aortic rings from SD rats which was inhibited by removal of the endothelium and by l-NAME (100 [mu]M) but not by indomethacin (10 [mu]M). The Ang-(1-7) receptor antagonist D-Pro7-Ang-(1-7) (0.1 [mu]M) abolished the vasodilator effect of the peptide. However, the other specific Ang-(1-7) receptor antagonist, A-779 in concentrations up to 10 [mu]M, did not affect vasodilation induced by Ang-(1-7). The Ang II AT1 and AT2 receptors antagonists CV11974 (0.01 [mu]M) and PD123319 (1 [mu]M), respectively, the bradykinin B2 receptor antagonist HOE 140 (1 [mu]M) and the inhibitor of ACE captopril (10 [mu]M) did not change the effect of Ang-(1-7). Our results show that in the aorta of SD rats, the vasodilator effect of Ang-(1-7) is dependent on endothelium-derived nitric oxide. This effect is mediated by the activation of Ang-(1-7) receptors sensitive to D-Pro7-Ang-(1-7), but not to A-779, which suggests the existence of a different Ang-(1-7) receptor subtype.
(C) 2007Elsevier, Inc.