The effects of temperature on cardiac E‐C coupling and intracellular Ca2+ buffering in trout cardiomyocytes

Abstract

To investigate the effects of acute temperature change on cardiac excitation‐contraction in fish heart, atrial and ventricular myocytes were isolated from rainbow trout acclimated to 12°C and studied using voltage clamp recording while simultaneously recording [Ca2+]i at 7°C, 14°C, and 21°C. Cells were stimulated in the presence or absence of sarcoplasmic reticulum (SR) inhibitors and SR Ca2+ load and intracellular Ca2+ buffering were determined with caffeine. Atrial and ventricular cells showed increased ICa density, faster ICa inactivation, and smaller gain at 14°C and 21°C compared to 7°C. SR inhibition was most effective at 7°C, where it decreased [Ca2+]i rise slope and amplitude by 58% and 44%, respectively, and prolonged recovery of [Ca2+]i by 1.6‐fold and decreased gain by 40%. An opposite trend emerged in ventricular cells in which SR inhibition had its largest effect at 21°C, where it decreased [Ca2+]i rise slope and amplitude by 60% and 75%, respectively, resulting in a 56% decrease in gain. Bmax for Ca2+ buffering did not differ between atrium and ventricle but was higher at 7°C (1392 ± 274 μM) than at 21°C (451 ± 274 μM) while Kd was unaffected by tissue or temperature (0.27 and 0.30 μM for atrium and ventricle, respectively). Thus, atrial myocytes show a particular sensitivity to cold and increased reliance on the SR to maintain [Ca2+]i in the face of reduce ICa, while ventricular myocytes do not. Maintained [Ca2+]i at cold temperatures in both cell types is maintained by a larger SR Ca2+ load.