Some ectothermic vertebrates show unusually good tolerance to oxygen shortage and it is therefore assumed that they might, as a defense mechanism, decrease number or activity of ion channels in order to reduce membrane leakage and thereby ATP-dependent ion pumping in hypoxia. Although several studies have provided indirect evidence in favor of this 'channel arrest' hypothesis, only few experiments have examined activity of ion channels directly from animals exposed to chronic hypoxia or anoxia in vivo. Here we compare the inwardly rectifying K(+) current (I(K1)), a major leak and repolarizing K(+) pathway of the heart, in cardiac myocytes of normoxic and hypoxic crucian carp, using the whole-cell and cell-attached single-channel patch-clamp methods. Whole-cell conductance of I(K1) was 0.5 +/- 0.04 nS/pF in normoxic fish and did not change during the 4 weeks hypoxic (O2 < 0.4 mg/l; 2.68 mmHg) period, meanwhile the activity of Na(+)/K(+)ATPase decreased 33%. Single-channel conductance of the I(K1) was 20.5 +/- 0.8 pS in control fish and 21.4 +/- 1.1 pS in hypoxic fish, and the open probability of the channel was 0.80 +/- 0.03 and 0.74 +/- 0.04 ( P > 0.05) in control and hypoxic fish, respectively. Open and closed times also had identical distributions in normoxic and hypoxic animals. These results suggest that the density and activity of the inward rectifier K(+) channel is not modified by chronic hypoxia in ventricular myocytes of the crucian carp heart. It is concluded that instead of channel arrest, the hypoxic fish cardiac myocytes obtain energy savings through 'action potential arrest' due to hypoxic bradycardia.