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
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