Hepatic metabolic and vascular responses to epinephrine: a unifying hypothesis

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Abstract
With the aid of rapid sampling techniques and measurements of phasic blood flow the complete time courses of epinephrine-induced hyperkalemia and hyperglycemia were delineated. The initial changes in transhepatic K and glucose balances and in the hepatic circulation were also determined. Efflux of K is coincident with the arrival of epinephrine at the liver, and is synchronous with or slightly earlier than glucose efflux. This implies that K and glucose release reflect a common epinephrine-sensitive process. Hyperkalemia is a transient phenomenon and is not sustained by the continued presence of the hormone. K efflux is independent of the initial decreases in total hepatic blood flow and in tissue oxygen tension induced by the hormone. We conclude that epinephrine initiates a sequence of reactions leading to glycogen breakdown, one of which results in an incidental loss of K. A hypothesis is suggested which accounts for efflux of both K and glucose on the basis of a single intracellular process.