The aim of the present study was to investigate the effects of high concentrations of KCl in releasing noradrenaline from sympathetic nerves and its actions on postsynaptic a-adrenoceptors. We measured the isotonic contractions induced by KCl in the isolated rat anococcygeus muscle under different experimental conditions. The contractile responses induced by KCl were inhibited by a-adrenoceptor antagonists in 2.5 mM Ca 2+ solution. Prazosin reduced the maximum effect from 100 to 53.9 ± 10.2%

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... 0.05) while the pD 2 values were not changed. The contractile responses induced by KCl were abolished by prazosin in Ca 2+ -free solution (P<0.05). Treatment of the rats with reserpine reduced the maximum effect induced by KCl as compared to the contractile responses induced by acetylcholine from 339.5 ± 157.8 to 167.3 ± 65.5% (P<0.05), and increased the pD 2 from 1.57 ± 0.01 to 1.65 ± 0.006 (P<0.05), but abolished the inhibitory effect of prazosin (P<0.05). In contrast, L-NAME increased the contractile responses induced by 120 mM KCl by 6.2 ± 2.3% (P<0.05), indicating that KCl could stimulate the neurons that release nitric oxide, an inhibitory component of the contractile response induced by KCl. Our results indicate that high concentrations of KCl induce the release of noradrenaline from noradrenergic neurons, which interacts with a 1adrenoceptors in smooth muscle cells, producing a contractile response in 2.5 mM Ca 2+ (100%) and in Ca 2+ -free solution, part of which is due to a direct effect of KCl on the rat anococcygeus muscle. Correspondence L.M. Bendhack Laboratório de Farmacologia FCFRP, USP Av. do Café, s/n 14040-903 Ribeirão Preto, SP Brasil