Hepatic metabolic and vascular responses to epinephrine: a unifying hypothesis

¹ Department of Physiology, The University of Rochester School of Medicine and Dentistry, Rochester, New York

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.

Key Words: carbohydrate and K metabolisms • hepatic circulation mechanism of hormone action

Submitted on April 11, 1963

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