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 exchanger inhibitor. Phenylephrine increased the L-type Ca 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 influx through the L-type Ca channel, and the concomitant increase in action potential duration acts as an enhancing factor.
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| http://dx.doi.org/10.3390/ijms24043926 | DOI Listing |
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