The significance of adrenaline-induced potentiation of electrogenic sodium pumping in bullfrog sympathetic ganglia

Abstract

Two different electrophysiological responses in amphibian sympathetic ganglia were studied by means of the sucrose gap technique; (i) the potassium-activated hyperpolarization (KH) which serves as an index of electrogenic Na+ pumping, and (ii) the hyperpolarization induced by adrenaline (AdH). Under appropriate experimental conditions, 0.1 μM adrenaline potentiated the KH to 121.5 ± 7.5% of control (n = 7). This potentiation was blocked by both yohimbine (50 nM) and prazosin (1 μM) but not by propranolol (1 μM). Clonidine (10 nM) potentiated the KH to 113.5 ± 3.4% of control (n = 5), whereas methoxamine (0.1 μM) was ineffective. Several lines of evidence argued against the hypothesis that the AdH may be generated, in whole or in part, by stimulation of the Na+ pump. For example, (i) the AdH was sometimes completely unaffected when the KH was blocked by ouabain, and (ii) the AdH was eliminated by 2 nM Ba2+ even though this cation enhanced membrane hyperpolarization accompanying electrogenic Na+ pumping. These results imply that the electrogenic Na+ pump is not involved in the short-term electrophysiological effects of catecholamines. Despite this, it is possible that the homeostasis of Na+ and K+ in nerve may be regulated by α-adrenergic mechanisms.