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+(K-ATP) channel, phosphodiesterase inhibitor, or C a2+ sensitizer on halothane-induced myocardial depression were investi gated in cultured rat ventricular myocytes. Halothane (1 to 4%) decrea sed the beating rate and amplitude in a dose-dependent manner. Myocard ial depressant effects of halothane were potentiated by the presence o f 10 nM nifedipine or verapamil. Neither cromakalim (1 mu M), glibencl amide (1 mu M), nor pimobendan (10 mu M) altered the dose-dependent de pressant effects of halothane. The mechanisms involving altered K-ATP channel, cAMP levels or Ca2+ sensitivity of contractile proteins may n ot be responsible for myocardial depression during halothane exposure. These results suggest that changes in L-type Ca2+ channel function pl ays an important role in the volatile anesthetic halothane-induced dep ression of contractile activity in cultured rat ventricular myocytes.