Gut sensing of potassium intake and its role in potassium homeostasis

Abstract

Extracellular K(+) homeostasis has been explained by feedback mechanisms in which changes in extracellular K(+) concentration drive renal K(+) excretion directly or indirectly via stimulating aldosterone secretion. However, this cannot explain meal-induced kaliuresis, which often occurs without increases in plasma K(+) or aldosterone concentrations. Recent studies have produced evidence supporting a feedforward control in which gut sensing of dietary K(+) increases renal K(+) excretion (and extrarenal K(+) uptake) independent of plasma K(+) concentrations, namely, a gut factor. This review focuses on these new findings and discusses the role of gut factor in acute and chronic regulation of extracellular K(+) as well as in the beneficial effects of high K(+) intake on the cardiovascular system.

Keywords: Potassium excretion; feedback control; feedforward control; potassium adaptation; potassium balance.

Figure 1

A schematic diagram illustrating feedback vs. feedforward control of K⁺ homeostasis.

Figure 2

A schematic figure illustrating the effects of plasma [K⁺] per seinsulin, and the hypothetical gut factor on the rise of plasma [K⁺] during K⁺ intake.

Figure 3

Changes in urinary K⁺ excretion with altered K⁺ intake. Rats were maintained on a control 1.0% K⁺ diet for 3 days, a modest K⁺-restricted (0.33% K⁺) diet for the following 3 days, and again the control diet for the final 3 days. Animals were individually housed and had free access to food only at night (6 PM – 6 AM). Urinary K⁺ excretion was determined for the absorptive (6 PM – 6 AM, night) and the postabsorptive (6 AM – 6 PM, day) periods. Data are means ± SE (n=4).

Figure 4

Schematic diagrams illustrating a decrease in renal K⁺ excretion after an overnight K⁺ deprivation (A) or its rapid reversal following an overnight feeding with a normal 1% K⁺ diet (B). In Athe gut factor effect (with 1% K⁺ meal) to enhance renal K⁺ excretion from previous feeding wanes over time, resulting in a profound decrease in K⁺ excretion after an overnight K⁺ restriction (0% K⁺ meal; i.e., without gut factor activation).