1962American Journal of Physiology-Legacy ContentRequires access

Effects of potassium and rubidium on muscle cell bicarbonate

James B. Hudson, Arnold S. Relman

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Abstract

A tissue CO2 content method was used to study the effects of Rb and K on skeletal muscle bicarbonate and pH in rats. Intraperitoneal injection of large loads of RbCl or KCl in normal rats produced extracellular acidosis and a transient intracellular alkalosis in muscle (and also in renal cortex). This supports previous suggestions that rapid exchange of administered cation for intracellular hydrogen occurs. In K-deficient alkalotic rats, loading with RbCl or KCl caused a greater fall in extracellular bicarbonate but a smaller rise in muscle bicarbonate. Muscle bicarbonate was unchanged by the alkalosis of K depletion or the reduction in extracellular bicarbonate resulting from chronic feeding of Rb. After the acute RbCl and KCl loads, repair of intracellular alkalosis occurred within 6 hr, associated with a transient sharp rise in tissue citrate content. It is suggested that production of citrate and other metabolic acids may play a role in stabilizing cellular acid-base balance.

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A tissue CO2 content method was used to study the effects of Rb and K on skeletal muscle bicarbonate and pH in rats. Intraperitoneal injection of large loads of RbCl or KCl in normal rats produced extracellular acidosis and a transient intracellular alkalosis in muscle (and also in renal cortex). This supports previous suggestions that rapid exchange of administered cation for intracellular hydrogen occurs. In K-deficient alkalotic rats, loading with RbCl or KCl caused a greater fall in extracellular bicarbonate but a smaller rise in muscle bicarbonate. Muscle bicarbonate was unchanged by the alkalosis of K depletion or the reduction in extracellular bicarbonate resulting from chronic feeding of Rb. After the acute RbCl and KCl loads, repair of intracellular alkalosis occurred within 6 hr, associated with a transient sharp rise in tissue citrate content. It is suggested that production of citrate and other metabolic acids may play a role in stabilizing cellular acid-base balance.

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Available abstract

A tissue CO2 content method was used to study the effects of Rb and K on skeletal muscle bicarbonate and pH in rats. Intraperitoneal injection of large loads of RbCl or KCl in normal rats produced extracellular acidosis and a transient intracellular alkalosis in muscle (and also in renal cortex). This supports previous suggestions that rapid exchange of administered cation for intracellular hydrogen occurs. In K-deficient alkalotic rats, loading with RbCl or KCl caused a greater fall in extracellular bicarbonate but a smaller rise in muscle bicarbonate. Muscle bicarbonate was unchanged by the alkalosis of K depletion or the reduction in extracellular bicarbonate resulting from chronic feeding of Rb. After the acute RbCl and KCl loads, repair of intracellular alkalosis occurred within 6 hr, associated with a transient sharp rise in tissue citrate content. It is suggested that production of citrate and other metabolic acids may play a role in stabilizing cellular acid-base balance.

Key concepts: Alkalosis, Bicarbonate, Metabolic alkalosis, Extracellular, Acidosis, Chemistry, Potassium, Intracellular pH

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