Ca2+-dependent K+ channels are targets for bradykinin B-1 receptor ligands and for lipopolysaccharide in the rat aorta

Ca2+-dependent K+ channels are targets for bradykinin B-1 receptor ligands and for lipopolysaccharide in the rat aorta

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 Although rat aorta smooth muscle cells in culture constitutively express bradykinin B, receptors, the normotensive rat aorta does not respond to the bradykinin B, receptor agonist des-Arg(9)-bradykinin, whereas vessels from the spontaneously hypertensive rat (SFIR) respond to bradykinin B, receptor agonists with cell membrane hyperpolarization and relaxation. Bacterial lipopolysaccharide also is inactive on the normotensive rat but hyperpolarizes the SFIR aorta. To determine whether this could be due to the increased intracellular Ca2+ concentration ([Ca2+](i)) in the SHR, we raised [Ca2+](i) in normotensive rats by treatment with thapsigargin. fit the thapsigargin-treated aorta, both lipopolysaccharide and des-Arg(9)-bradykinin induced hyperpolarization, which was reversed by the Ca2+-dependent K+ channel inhibitor iberiotoxin and by the bradykinin B, receptor antagonists Lys-[Leu(8)]-des-Arg(9)-bradykinin and [Leu(8)]-des-Arg9-bradykinin. Thus the bradykinin B-1 receptor, as well as lipopolysaccharide, needs activated Ca2+-dependent K+ channels for functional expression. the two bradykinin B-1 receptor inhibitors, however, have effects oil Ca2+-dependent K+ channels which are not mediated by bradykinin B, receptors. (c) 2005 Elsevier B.V. All rights reserved.
Keywords bradykinin B-1 receptor
lipopolysaccharide
(rat) aorta
calcium-dependent K+ channel
Language English
Date 2005-11-21
Published in European Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 525, n. 1-3, p. 123-127, 2005.
ISSN 0014-2999 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 123-127
Origin http://dx.doi.org/10.1016/j.ejphar.2005.09.047
Access rights Closed access
Type Article
Web of Science ID WOS:000233711400019
URI http://repositorio.unifesp.br/handle/11600/28553

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