Lys-[Leu(8),des-Arg(9)]-bradykinin blocks lipopolysaccharide-induced SHR aorta hyperpolarization by inhibition of Ca++- and ATP-dependent K+ channels

Lys-[Leu(8),des-Arg(9)]-bradykinin blocks lipopolysaccharide-induced SHR aorta hyperpolarization by inhibition of Ca++- and ATP-dependent K+ channels

Author Farias, N. C. Google Scholar
Feres, T. Google Scholar
Paiva, ACM Google Scholar
Paiva, T. B. Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Abstract The mediators involved in the hyperpolarizing effects of lipopolysaccharide and of the bradykinin B, receptor agonist des-Arg(9)-bradykinin on the rat aorta were investigated by comparing the responses of aortic rings of spontaneously hypertensive and normotensive Wistar rats. Endothelized rings from hypertensive rats were hyperpolarized by des-Arg(9)-bradykinin and lipopolysaccharide, whereas deendothelized rings responded to lipopolysaccharide but not to des-Arg(9)-bradykinin. in endothelized preparations, the responses to des-Arg(9)-bradykinin were inhibited by N-nitro-L-arginine and iberiotoxin. De-endothelized ring responses to lipopolysaccharide were inhibited by iberiotoxin, glibenclamide and B, antagonist Lys-[Leu(8),des-Arg(9)]-bradykinin. This antagonist also inhibited hyperpolarization by des-Arg(9)-bradykinin and by the a(2)-adrenoceptor agonist, brimonidine. Our results indicate that Ca2+-sensitive K+ channels are the final mediators of the responses to des-Arg(9)-bradykinin, whereas both Ca2+- and ATP-sensitive K+ channels mediate the responses to lipopolysaccharide. the inhibitory effects of Lys-[Leu(8),des-Arg(9)]-bradykinin is due to a direct action on Ca2+- and ATP-sensitive potassium channels. (C) 2004 Elsevier B.V All rights reserved.
Keywords des-Arg(9)-bradykinin
lipopolysaccharide
rat, spontaneously hypertensive
aorta
K+ channel
Language English
Date 2004-09-13
Published in European Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 498, n. 1-3, p. 163-169, 2004.
ISSN 0014-2999 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 163-169
Origin http://dx.doi.org/10.1016/j.ejphar.2004.07.002
Access rights Closed access
Type Article
Web of Science ID WOS:000224044100023
URI http://repositorio.unifesp.br/handle/11600/27937

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