Temperature acclimation modifies sinoatrial pacemaker mechanism of the rainbow trout heart (original) (raw)

Haverinen J, Vornanen M. Temperature acclimation modifies sinoatrial pacemaker mechanism of the rainbow trout heart. The hypothesis of pacemaker level origin of thermal compensation in heart rate was tested by recording action potentials (AP) in intact sinoatrial tissue and enzymatically isolated pacemaker cells of rainbow trout acclimated at 4°C (cold) and 18°C (warm). With electrophysiological recordings, the primary pacemaker was located at the base of the sinoatrial valve, where a morphologically distinct ring of tissue comprising myocytes and neural elements was found by histological examination. Intrinsic beating rate of this pacemaker was higher in cold-acclimated (46 Ϯ 6 APs/min) than warm-acclimated trout (38 Ϯ 3 APs/min; P Ͻ 0.05), and a similar difference was seen in beating rate of isolated pacemaker cells (44 Ϯ 6 vs. 38 Ϯ 6 APs/min; P Ͻ 0.05), supporting the hypothesis that thermal acclimation modifies the intrinsic pacemaker mechanism of fish heart. Inhibition of sarcoplasmic reticulum (SR) with 10 M ryanodine and 1 M thapsigargin did not affect heart rate in either warm-or coldacclimated trout at 11°C but reduced heart rate in warm-acclimated trout from 74 Ϯ 2 to 42 Ϯ 6 APs/min (P Ͻ 0.05) at 18°C. At 11°C, a half-maximal blockade of the delayed rectifier K ϩ current (IKr) with 0.1 M E-4031 reduced heart rate more in warm-acclimated (from 45 Ϯ 1 to 24 Ϯ 5 APs/min) than cold-acclimated trout (56 Ϯ 3 vs. 48 Ϯ 2 APs/min), whereas IKr density was higher and AP duration less in cold-acclimated trout (P Ͼ 0.05). Collectively, these findings suggest that a cold-induced increase in AP discharge frequency is at least partly due to higher density of the IKr in the cold-acclimated trout, whereas contribution of SR Ca 2ϩ release to thermal compensation of heart rate is negligible.