INCREASES IN URINARY KALLIKREIN ACTIVITY AND PROSTANOID SYNTHESIS AFTER DIETARY POTASSIUM SUPPLEMENTATION

SUMMARY 1. To determine whether increasing dietary potassium alters kallikrein activity or prostaglandin synthesis, 77 women participated in a 3 week screening to assess their dietary potassium intake. Forty‐four normotensive women whose dietary potassium was less than 60 mmol/day were allocated randomly to one of two groups who took either 80 mmol/day KC1 (Slow‐K, Ciba Geigy) or matching placebo for the first or second of two 4 week periods. 2. Significant increases in urinary kallikrein excretion (P < 0.01), and urinary 6‐keto‐PGF1α (P < 0.01) were observed during potassium supplementation. These changes occurred without alterations in urine volume or sodium excretion. 3. It is suggested that potassium‐induced changes in urinary 6‐keto‐PGF1α may reflect increased renal and possibly vascular synthesis of prostacyclin. These increases may be mediated by increased plasma potassium stimulating kallikrein synthesis, leading to bradykinin‐induced activation of phospholipase A2. Enhanced kallikrein/kinin and prostacyclin formation could contribute to the blood pressure lowering effect of potassium reported in hypertensive subjects.