Regulation of action potential duration under acute heat stress by IK,ATP and IK1 in fish cardiac myocytes

The mechanism underlying temperature-dependent shortening of action potential (AP) duration was examined in the fish ( Carassius carassius L.) heart ventricle. Acute temperature change from +5 to +18 degreesC ( heat stress) shortened AP duration from 2.8 +/- 0.3 to 1.3 +/- 0.1 s in intact ventricles. In 56% (18 of 32) of enzymatically isolated myocytes, heat stress also induced reversible opening of ATP-sensitive K+ channels and increased their single-channel conductance from 37 +/- 12 pS at +8degreesC to 51 +/- 13 pS at +18 degreesC (Q(10) = 1.38) (P < 0.01; n = 12). The ATP-sensitive K+ channels of the crucian carp ventricle were characterized by very low affinity to ATP both at +8 °C [concentration of Tris-ATP that produces half-maximal inhibition of the channel (K-1/2) = 1.35 mM] and +18 °C (K-1/2 = 1.85 mM). Although acute heat stress induced ATP-sensitive K+ current (I-K,I-ATP) in patch-clamped myocytes, similar heat stress did not cause any glibenclamide (10 μM)-sensitive changes in AP duration in multicellular ventricular preparations. Examination of APs and K+ currents from the same myocytes by alternate recording under current-clamp and voltage-clamp modes revealed that changes in AP duration were closely correlated with temperature-specific changes in the voltage-dependent rectification of the background inward rectifier K+ current I-K1. In ∼15% of myocytes (4 out of 27), I-K,I-ATP-dependent shortening of AP followed the I-K1-induced AP shortening. Thus heat stress-induced shortening of AP duration in crucian carp ventricle is primarily dependent on I-K1. I-K,I-ATP is induced only in response to prolonged temperature elevation or perhaps in the presence of additional stressors.