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Am J Physiol Regul Integr Comp Physiol 286: R405-R415, 2004. First published October 30, 2003; doi:10.1152/ajpregu.00500.2003
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INFLAMMATION, CYTOKINES, AND TEMPERATURE REGULATION

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

Vesa Paajanen and Matti Vornanen

Department of Biology, University of Joensuu, 80101 Joensuu, Finland

Submitted 29 August 2003 ; accepted in final form 28 October 2003

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°C (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 +8°C to 51 ± 13 pS at +18°C (Q10 = 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 (K1/2)= 1.35 mM] and +18°C (K1/2 = 1.85 mM). Although acute heat stress induced ATP-sensitive K+ current (IK,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 IK1. In ~15% of myocytes (4 out of 27), IK,ATP-dependent shortening of AP followed the IK1-induced AP shortening. Thus heat stress-induced shortening of AP duration in crucian carp ventricle is primarily dependent on IK1. IK,ATP is induced only in response to prolonged temperature elevation or perhaps in the presence of additional stressors.

inward rectifier potassium current; adenosine 5'-triphosphate-sensitive potassium current; fish heart; temperature



Address for reprint requests and other correspondence: V. Paajanen, Univ. of Joensuu, Dept. of Biology, P.O. Box 111, 80101 Joensuu, Finland (E-mail address: vpaajane{at}cc.joensuu.fi).




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