Role of L-type calcium channels on halothane-induced myocardial depression in cultured rat ventricular myocytes.

The effects of antagonists for L-type Ca2+ channel, opener and blocker to ATP-sensitive K+ (KATP) channel, phosphodiesterase inhibitor, or Ca2+ sensitizer on halothane-induced myocardial depression were investigated in cultured rat ventricular myocytes. Halothane (1 to 4%) decreased the beating rate and amplitude in a dose-dependent manner. Myocardial depressant effects of halothane were potentiated by the presence of 10 nM nifedipine or verapamil. Neither cromakalim (1 microM), glibenclamide (1 microM), nor pimobendan (10 microM) altered the dose-dependent depressant effects of halothane. The mechanisms involving altered KATP channel, cAMP levels or Ca2+ sensitivity of contractile proteins may not be responsible for myocardial depression during halothane exposure. These results suggest that changes in L-type Ca2+ channel function plays an important role in the volatile anesthetic halothane-induced depression of contractile activity in cultured rat ventricular myocytes.