KALIURESIS IN NORMAL SUBJECTS FOLLOWING ORAL POTASSIUM CITRATE INTAKEWITHOUT INCREASED PLASMA POTASSIUM CONCENTRATION

Ingestion of potassium salts typically induces both a kaliuresis and a n increase in the systemic plasma potassium concentration. In this stu dy normal healthy adults undergoing water diuresis ingested potassium citrate or sodium citrate (0.5 mmol/kg body weight) or continued witho ut ion ingestion (a time control group). Urine was collected over 20-m in intervals and venous blood sampled at midinterval. Intake of potass ium citrate led to a significant increase in potassium excretion that began during the first postingestion collection and peaked 60-80 min a fter intake with a maximal increase in potassium excretion above basel ine of 1.60 mu mol/min . kg(-1). The kaliuresis occurred without chang es in plasma potassium concentration, excretion of creatinine or calci um, or urine hypo-osmolality and was associated with a briefer, smalle r, and less regular increase in sodium excretion and a pronounced but irregular increase in chloride excretion. Plasma aldosterone was insig nificantly elevated above baseline, and the initial increase did not o ccur until 40-60 min after potassium intake. Intake of sodium citrate did not produce a kaliuresis. The cause of the kaliuresis does not app ear to be an increased systemic plasma potassium concentration, an inc reased plasma level of aldosterone, intake of citrate, or an elevated excretion of sodium. The mechanism inducing the kaliuresis following o ral potassium intake in the absence of changes in systemic plasma pota ssium may involve a reflex initiated at potassium sensors in gut, port al vein, or liver.