Effects of moderate short-term potassium depletion in normal humans. The role of prostaglandins.

The role of prostaglandins (PG) in the effects of potassium (K+)depletion was studied in six normal women. A mean K+-deficit of 220 mEq was induced with and without concomitant treatment with indomethacin (150 mg/day). Mean serum K+ concentration decreased from 4.2 +/- (S.E.) 0.1 to 3.2 +/- 0.1 mEq/L without indomethacin and from 4.1 +/- 0.1 to 3.2 +/- 0.1 mEq/L with indomethacin. "Supine" and "upright" plasma renin activity (PRA) and plasma norepinephrine concentration (NE) were unaltered by K+ -depletion alone but decreased with indomethacin. Plasma aldosterone (PA) was suppressed during K+-depletion (control: 7.2 +/- 2.6 ng/dl supine, 19.3 +/- 8.1 ng/dl upright; K+-depletion: 2.6 +/- 0.3 ng/dl supine, 5.5 +/- 1.3 ng/dl upright) and was paralleled by a decrease in urinary aldosterone. K+- depletion decreased urinary PGE2 from 667 +/- 133 to 343 +/- 60 ng/day (P less than 0.025) without a change in PGF2 alpha. The dose of exogenous angiotensin II (A II) which increased diastolic blood pressure by 20 mm Hg (pressor dose) was 7.1 +/- 1.4 ng/kg/min during control and increased to 11.0 +/- 0.7 ng/kg/min during K+-depletion (P less than 0.05). Indomethacin increased the sensitivity to A II both during control (pressor dose: 4.9 +/- 0.6 ng/kg/min) and K+ - depletion (pressor dose: 6.0 +/- 1.0 ng/kg/min). These results indicate that in healthy subjects, moderate short-term K+-depletion does not affect PRA or NE but decreases production of aldosterone and PGE2 by the kidney. The changes in vascular sensitivity to exogenous A II during K+-depletion and indomethacin and the decreases in plasma NE and PRA during indomethacin may be explained by changes in vascular vasodilator PG.