OBJECTIVETo understand the effect of pinacidil on rat myocardial Ca(2+)regulation.

METHODSAfter baseline measurement and a period of equilibrium, myocytes were randomly allocated to one of 4 treatment groups: Control group (8 myocytes): incubation in Lactate Ringer's solution at 24 degrees C for 2 hours; K group (8 myocytes): incubation in Lactate Ringer's solution containing 16 mmol/L potassium at 24 degrees C for 2 hours; K+P group (8 myocytes): incubation in Lactate Ringer's solution containing potassium 16 mmol/L and pinacidil 50 micromol/L at 24 degrees C for 2 hours; K+P+G group (8 myocytes): incubation in Lactate Ringer's solution containing potassium 16 mmol/L, pinacidil 50 micromol/L and glibenclamide 10 micromol/L at 24 degrees C for 2 hours. After each incubation, myocytes were resuspended in cell culture media at the same temperature and intracellular [Ca(2+)](i) and SR Ca(2+) release were measured.

RESULTSThe amplitude percent of [Ca(2+)](i) transient evoked by electrical stimulation in the K group was significantly decreased to 67.05% - 80.11% compared to 90.27% - 95.57% in the K+P group during reperfusion after ischemia (P<0.01). The percent amplitude of the [Ca(2+)](i) transient evoked by the rapid application of 10 mmol caffeine in the K group myocyte was approximately 112.00%+/-16.93% compared with that of the [Ca(2+)](i) transient evoked by electrical stimulation. However, in the K+P group myocyte the peak amplitude of the caffeine induced Ca(2+) release was 173.15%+/-26.01% compared with electrical stimulation (P<0.01). The duration of transient evoked by caffeine in K+P group (3.20+/-0.71 ms was significantly shorter than that in K group (3.93+/-0.46) ms (P<0.05).

CONCLUSIONCardioplegic arrest with simultaneous activation of KATP channels preserves rat myocardial Ca2+ by inducing sarcoplasmic reticulum Ca(2+) release and by alteration of Na(+)-Ca(2+) exchanger to better maintain [Ca(2+)](i) homeostasis.