Potassium depletion induced by dietary potassium restriction is known to cause sodium retention, while potassium supplementation is known to increase urinary sodium excretion. However, the ability of potassium deficiency to affect mineralocorticoid-induced sodium retention in aldosterone-producing adenoma (APA) subjects has not been extensively investigated, neither in baseline conditions nor when facilitating natriuresis through a physiological manoeuver such as central blood volume expansion. With the aim of testing the hypothesis that potassium supplementation would attenuate the mineralocorticoid-induced sodium retention, in 7 APA patients elevation of serum potassium was obtained by infusion of isosmotic potassium chloride (KCl) at a constant rate of 36 mmol/h for a 2-hour period for 5 consecutive days. The same patients were also submitted to acute central volume expansion by head-out water immersion (WI) associated with either low or normal serum potassium levels. The assessment of natriuresis in baseline condition and during Wl was also performed in 10 age-matched control subjects. Central hypervolemia by WI induced a significant natriuretic response in APA hypokalemic subjects; on the other hand, in the same APA subjects giving potassium supplementation, WI-induced urinary sodium excretion was significantly higher (P <.001) than that obtained during WI at normal potassium intake (hypokalemic condition). Blood pressure responses and hormonal profiles were almost superimposable during the 2 WI experiments performed at different serum potassium levels. By confirming that amelioration of hypokalemia attenuates mineralocorticoid-induced sodium retention, this study also suggests that potassium intake may represent an important determinant of mineralocorticoid escape.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism