The function of the sarcoplasmic reticulum is not inhibited by low temperatures in trout atrial myocytes.

Abstract

The effect of temperature on sarcoplasmic reticulum (SR) Ca(2+) uptake and release was measured in trout atrial myocytes using the perforated patch-clamp technique. Depolarization of the myocyte for 10 s to different membrane potentials (V(m)) induced SR Ca(2+) uptake. The relationship between V(m) and SR Ca(2+) uptake was not significantly changed by lowering the experimental temperature from 21 to 7 degrees C, and the relationship between total cytosolic Ca(2+) and SR Ca(2+) uptake was similar at the two temperatures with a pooled V(max) = 66 amol/pF and K(0.5) = 4 amol/pF. Quantification of the Ca(2+) release from the SR elicited by 10-ms depolarizations to different V(m) showed an increasing SR Ca(2+) release at more positive V(m) between -50 and +10 mV, whereas SR Ca(2+) release stagnated between +10 and +50 mV. Lowering of the temperature did not affect this relationship significantly, giving an SR Ca(2+) release of 1.71 and 1.54 amol/pF at 21 and 7 degrees C, respectively. Furthermore, clearance of the SR Ca(2+) content slowed down inactivation of the L-type Ca(2+) current at both temperatures (the fast time constant increased significantly from 10.4 +/- 1.9 to 15.0 +/- 2.0 ms at 21 degrees C and from 38 +/- 15 to 73 +/- 24 ms at 7 degrees C). Thus the SR has the capacity to remove the entire Ca(2+) transient at physiologically relevant stimulation frequencies at both 21 and 7 degrees C, although it is estimated that ~40% of the total Ca(2+) transient is liberated from and reuptaken by the SR with continuous stimulation at 0.5 Hz independently of the experimental temperature.