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Am J Physiol Cell Physiol 258: C24-C29, 1990;
0363-6143/90 $5.00
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AJP - Cell Physiology, Vol 258, Issue 1 C24-C29, Copyright © 1990 by American Physiological Society

ARTICLES

Alanine stimulation of passive potassium efflux in hepatocytes is independent of Na(+)-K+ pump activity

B. J. Cohen and C. Lechene
Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02115.

We have studied the effects of alanine on electrolyte content and ion transport in rat hepatocytes in primary culture. Application of 10 mM alanine is followed by 1) an increase in the rate of sodium entry; 2) an increase in intracellular sodium content; 3) an increase in ouabain-inhibitable rubidium uptake, a measure of Na(+)-K+ pump rate; 4) an increase in unidirectional potassium efflux, whether or not the Na(+)-K+ pump was inhibited; and 5) an increase in the initial rate of potassium loss after Na(+)-K+ pump inhibition. This increase occurred even when alanine was presented in Ringer made hypertonic by the addition of sucrose. Application of hypotonic solution led to a significant net loss of potassium, but no net loss of potassium was observed after alanine application. Thus alanine stimulates the Na(+)-K+ pump by increasing intracellular sodium secondary to an increase in the rate of sodium entry. Passive potassium efflux is stimulated by a mechanism that is independent of the stimulation of the Na(+)-K+ pump. The stimulated potassium efflux does not appear to be a response to cell swelling.


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