Regulation of renal K transport by dietary K intake

Abstract

Extracellular K must be kept within a narrow concentration range for the normal function of neurons, skeletal muscle, and cardiac myocytes. Maintenance of normal plasma K is achieved by a dual mechanism that includes extrarenal factors such as insulin and beta-adrenergic agonists, which stimulate the movement of K from extracellular to intracellular fluid and modulate renal K excretion. Dietary K intake is an important factor for the regulation of K secretion: An increase in K intake stimulates secretion, whereas a decrease inhibits K secretion and enhances absorption. This effect of changes in dietary K intake on tubule K transport is mediated by aldosterone-dependent and -independent mechanisms. Recently, it has been demonstrated that the protein tyrosine kinase (PTK)-dependent signal transduction pathway is an important aldosterone-independent regulatory mechanism that mediates the effect of altered K intake on K secretion. A low-K intake stimulates PTK activity, which leads to increase in phosphorylation of cloned inwardly rectifying renal K (ROMK) channels, whereas a high-K intake has the opposite effect. Stimulation of tyrosine phosphorylation also suppresses K secretion in principal cell by facilitating the internalization of apical K channels in the collecting duct.