Acute Temperature Change Modulates the Response of ICa to Adrenergic Stimulation in Fish Cardiomyocytes

The purpose of this study was to investigate how the endogenous catecholamine adrenaline protects sarcolemmal Ca2+ flux through the L-type Ca2+ channel (ICa) during acute exposure to cold in the fish heart. We examined the response of ICa to adrenergic stimulation at three temperatures (7°, 14°, and 21°C) in atrial myocytes isolated from rainbow trout acclimated to 14°C. We found that ICa amplitude varied directly with test temperature and was increased by adrenergic stimulation (AD; 5 nM and 1 μM) at all temperatures. However, ICa was significantly more sensitive to adrenergic stimulation at the coldest test temperature. In fact, at 7°C in the absence of AD, ICa was extremely low. The addition of 1 μM AD increased peak ICa 7.2-fold at 7°C, 2.6-fold at 14°C, and 1.6-fold at 21°C and ameliorated the temperature-dependent difference in Ca2+ influx across the cell membrane. We suggest that this increased adrenergic sensitivity is a critical compensatory mechanism that allows the rainbow trout heart to maintain contractility during acute exposure to cold temperatures. In particular, the tonic level of adrenergic stimulation provided by circulating plasma catecholamines (i.e., in the nM concentration range) may be crucial for effective excitation-contraction coupling in the cold cardiomyocyte.