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

Autor Farias, N. C. Google Scholar
Feres, T. Google Scholar
Paiva, ACM Google Scholar
Paiva, T. B. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo 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.
Palavra-chave des-Arg(9)-bradykinin
lipopolysaccharide
rat, spontaneously hypertensive
aorta
K+ channel
Idioma Inglês
Data de publicação 2004-09-13
Publicado em European Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 498, n. 1-3, p. 163-169, 2004.
ISSN 0014-2999 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 163-169
Fonte http://dx.doi.org/10.1016/j.ejphar.2004.07.002
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000224044100023
Endereço permanente http://repositorio.unifesp.br/handle/11600/27937

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