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

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 [Ca 2+ ] i at 7°C, 14°C, and 21°C. Cells were stimulated in the presence or absence of sarcoplasmic reticulum (SR) inhibitors and SR Ca 2+ load and intracellular Ca 2+ buffering were determined with caffeine. Atrial and ventricular cells showed increased I Ca density, faster I Ca 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 [Ca 2+ ] i rise slope and amplitude by 58% and 44%, respectively, and prolonged recovery of [Ca 2+ ] 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 [Ca 2+ ] i rise slope and amplitude by 60% and 75%, respectively, resulting in a 56% decrease in gain. B max for Ca 2+ 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 K d 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 [Ca 2+ ] i in the face of reduce I Ca , while ventricular myocytes do not. Maintained [Ca 2+ ] i at cold temperatures in both cell types is maintained by a larger SR Ca 2+ load.