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

Two different electrophysiological responses in amphibian sympathetic ganglia were studied by means of the sucrose gap technique; the potassium-activated hyperpolarization (KH) which serves as an index of electrogenic Na+ pumping, and the hyperpolarization induced by adrenaline (AdH). Under appropriate experimental conditions, 0.1 microM 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 microM) but not by propranolol (1 microM). Clonidine (10 nM) potentiated the KH to 113.5 +/- 3.4% of control (n = 5), whereas methoxamine (0.1 microM) 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, the AdH was sometimes completely unaffected when the KH was blocked by ouabain, and the AdH was eliminated by 2 mM 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 alpha-adrenergic mechanisms.