Effects of pH on potassium: new explanations for old observations

Abstract

Maintenance of extracellular K(+) concentration within a narrow range is vital for numerous cell functions, particularly electrical excitability of heart and muscle. Potassium homeostasis during intermittent ingestion of K(+) involves rapid redistribution of K(+) into the intracellular space to minimize increases in extracellular K(+) concentration, and ultimate elimination of the K(+) load by renal excretion. Recent years have seen great progress in identifying the transporters and channels involved in renal and extrarenal K(+) homeostasis. Here we apply these advances in molecular physiology to understand how acid-base disturbances affect serum potassium.

Figure 1.

K⁺ concentration in the extracellular fluid (ECF) is affected by dietary intake, exchange with the intracellular fluid (ICF), and urinary excretion.

Figure 2.

Multiple ion transport pathways directly or indirectly affect net K⁺ flux in skeletal muscle cells.

Figure 3.

Apparent K⁺-H⁺ exchange (or K⁺-HCO₃⁻ cotransport) in skeletal muscle cells can arise from functional coupling between (A) Na⁺-H⁺ exchange and Na⁺,K⁺-ATPase, (B) Na⁺-HCO₃⁻ cotransport and Na⁺,K⁺-ATPase, or (C) Cl⁻-HCO₃⁻ exchange and K⁺-Cl⁻ cotransport.

Figure 4.

Opposing effects of extracellular and intracellular pH modify the influence of organic acidosis on plasma K⁺.

Figure 5.

Urinary K⁺ excretion is the resultant of filtration, reabsorption and secretion along the nephron. Mechanisms of K⁺ transport in proximal tubule, thick ascending limb, and distal nephron (connecting and collecting tubule) are shown in the inset.

Figure 6.

Multiple ion transport pathways directly or indirectly affect K⁺ transport in the connecting tubule and cortical collecting tubule and are affected by pH.