Examination of the role of the electrogenic sodium pump in the adrenaline‐induced hyperpolarization of amphibian neurones.

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Abstract
The effect of adrenaline [epinephrine] and acetylcholine (ACh) on the membrane potential of R. pipiens sympathetic ganglia was examined by means of the sucrose gap recording technique. Adrenaline (1-50 .mu.M) consistently produced a hyperpolarization (Adrh) which was not reduced by Ringer solution containing 10 mM-Mn2+, nor by Ringer solution where the Na+ concentration was reduced from 100 to 30 mM. High doses of ACh (10 mM) produced a biphasic response, a depolarization (AChd) followed by an after-hyperpolarization (ACha.h.p.). Ringer solution containing 100 mM-Li+ (rather than 100 mM-Na+) or 10 .mu.M ouabain blocked the ACha.h.p. and reduced the Adrh. The AChd was essentially unchanged. Ringer solution containing 0.2 mM-K+ (rather than 2 mM-K+) blocked part of the ACha.h.p. whereas the Adrh was enhanced. Ringer solution containing 6 mM-K+ reduced the amplitude of the Adrh. The Adrh and the antidromically evoked action potential after-hyperpolarization (antidromic a.h.p.) reversed polarity at approximately the same membrane potential. These data do not support the hypothesis that the Adrh results from activation of the electrogenic Na pump. The response may be generated by an increase in K conductance (gK) which is especially sensitive to manipulations which result in Na pump inhibition.