Do catecholamines directly modulate the delayed plateau potassium current in frog atrium?

An important electrophysiological action of catecholamines in the heart is the modulation of the second inward current (iCa). Catecholamine augmentation of iCa has been attributed to an increase in the number of functional channels, as well as an increase in the probability of channel opening [1, 4, 12]. Another important electrophysiological action of catecholamines in the heart is the modulation of time-dependent outward currents. In the Purkinje fibre, epinephrine has been shown to shift the voltage-dependence of the pacemaker current, iK2 [13]. The delayed outward current(s) which is activated over the plateau range of potentials (ix) is also augmented by catecholamines in Purkinje fibers [14] as well as frog atrium [3]. Several possible mechanisms for enhancement of the outward plateau current by catecholamines have been proposed [2]: (i) a direct increase in the maximal conductance of the channel; (ii) an indirect enhancement of outward current mediated by stimulation of Na+-K+ exchange (which may reduce potassium concentration in restricted extracellular spaces and hence produce an increase in the driving force for K+) or (iii) an indirect augmentation of outward current via enhancement of intracellular Ca2+ (calcium-activated potassium conductance) [10]. To distinguish between these possible mechanisms, the influence of epinephrine and isoproterenol on the delayed outward K+ current in single isolated bullfrog atrial cells was examined. Evidence is presented that in single frog atrial cells, concentrations of epinephrine or isoproterenol which produce large increases in the second inward current have no detectable effect upon the delayed plateau K+ current.