Abstract
Mechanisms for the α-adrenoceptor-mediated positive inotropy in neonatal mouse ventricular myocardium were studied with isolated myocardial preparations. The phenylephrine-induced positive inotropy was suppressed by prazosin, nifedipine, and chelerythrine, a protein kinase C inhibitor, but not by SEA0400, a selective Na(+)/Ca(2+) exchanger inhibitor. Phenylephrine increased the L-type Ca(2+) channel current and prolonged the action potential duration, while the voltage-dependent K(+) channel current was not influenced. In the presence of cromakalim, an ATP-sensitive K(+) channel opener, the phenylephrine-induced prolongation of action potential duration, as well as the positive inotropy, were smaller than in the absence of cromakalim. These results suggest that the α-adrenoceptor-mediated positive inotropy is mediated by an increase in Ca(2+) influx through the L-type Ca(2+) channel, and the concomitant increase in action potential duration acts as an enhancing factor.