Depolarization produced by catecholamines in guinea-pig ventricular muscle cells exposed to potassium-rich media and its dependence on temperature.

Catecholamines (isoproterenol, adrenaline, and noradrenaline) elicited a small decrease in the resting potential of guinea-pig ventricular muscle cells depolarized by 27 mM K. This catecholamine-induced depolarization (CAD) was enhanced and often led to an automatic activity, when the membrane shunting conductance was reduced by application of 0.05 to 0.2 mM Ba. CAD was blocked by Mn (1 to 2 mM), verapamil (0.5 to 1 X 10(-5) M), and propranolol (0.1 to 1 X 10(-5) M), but not by phentolamine (10(-5) M). CAD did not develop when both Ca and Ba were absent in the bathing solution, but persisted when Sr was present. These results are consistent with the hypothesis that CAD was due at least partly to an increase in the slow channel conductance that was initiated by catecholamine/beta-receptor interaction. CAD was markedly enhanced at low temperatures (21 to 25 degrees C), and such was characterized by slow repolarization after drug withdrawal. Propranolol, when applied after catecholamine, exerted no appreciable effect on this slow repolarization. This beta-blocker abolished CAD at low temperature, if applied prior to catecholamine. Methylxanthines (2 to 5 mM caffeine or theophylline) produced a depolarization similar to that seen with CAD, and the rate of repolarization after drug withdrawal also slowed at low temperature. The slow repolarization of CAD at low temperature appeared to reflect a slowing in the postreceptor metabolic processes responsible for deactivation of the slow channel that was sensitive to beta-receptor stimulation.