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KATP channels mediate the β2-adrenoceptor agonist-induced relaxation of rat detrusor muscle.

By Diane Hudman, Ruth A. Elliott and Robert I. Norman

Abstract

This paper was published as European Journal of Pharmacology, 2000, 397 (1), pp. 169-176. It is available from http://www.sciencedirect.com/science/journal/00142999. Doi: 10.1016/S0014-2999(00)00229-6Metadata only entryWe propose that ATP-sensitive K+ (KATP) channels are normally inactive but involved in β2-adrenoceptor stimulated relaxation of the rat bladder. Spontaneous detrusor muscle contractions were unaffected by glibenclamide (KATP channel blocker) but were reduced when pinacidil (KATP channel opener) concentrations exceeded 10−5 M. Inhibition by β2-adrenoceptor agonist clenbuterol (10−6 M) of 1 Hz electrical field stimulated contractions was abolished by glibenclamide (10−6 M). Glibenclamide (10−6 M) decreased forskolin-induced relaxation (10−9–10−4 M) in bladder muscle stimulated with 1 Hz electrical field. In the presence glibenclamide (10−6 M) or myristoylated protein kinase A inhibitor (2×10−6 M), clenbuterol (10−9–10−5 M) failed to inhibit bladder contraction in response to 1 Hz electrical field stimulation. Therefore, KATP channel opening and the subsequent hyperpolarization of cell membranes in response to β2-adrenoceptor activation is mediated by raised cyclic-AMP levels and activation of protein kinase A. This counteracts ATP-stimulated depolarization in bladder muscle, thereby reducing cell contraction

Publisher: Elsevier
Year: 2000
DOI identifier: 10.1016/S0014-2999(00)00229-6
OAI identifier: oai:lra.le.ac.uk:2381/8945
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