Potassium supplementation lowers blood pressure and increases urinary kallikrein in essential hypertensives

In order to elucidate possible mechanism(s) involved in the blood pressure reduction induced by potassium (K) supplementation, we studied the changes of BP and of some of its regulatory systems, including levels of urinary kallikrein (UKal) - an index of renal kallikrein production. Twenty-four untreated essential hypertensives, with a basal BP of 147/96 ± 13/7 mmHg and normal renal function, received in crossover, double-blind, randomised fashion, 64 mmol KCl or placebo during two periods of 4 weeks each. At the 4th week of potassium supplementation systolic, diastolic and mean BPs decreased by 6.3 ± 2 (P < 0.01), 3.0 ± 2 and 4.1 ± 2 (P < 0.05) mmHg respectively for the supine position, and 5.0 ± 2, 4.0 ± 2 (P < 0.05) and 4.0 ± 1 (P < 0.05) mmHg for the standing position. Urinary potassium (K) increased from 55 ± 4 to 123 ± 6 mmol/24 hours (P < 0.001) and UKal from 692 ± 69 to 1052 ± 141 mU/24 hours (P < 0.01). Serum K rose from 3.8 ± 0.1 mEq/l to 4.1 ± 0.1 mmol/l (P < 0.001) and PRA from 0.77 ± 0.12 to 0.99 ± 0.14 ng/ml/h (P < 0.05). Correlations were observed between UKal and urinary K (r = 044, P < 0.0001); between differences in UKal and urinary K and in UKal and urinary Na (r = 0.50, P < 0.0005 and r = 0.48, P < 0.001 respectively). Responders to KCl supplementation (n = 7) had a greater increase of urinary kallikrein (P < 0.005) and PRA (P < 0.05) than nonresponders (n = 8). The present study confirms the mild BP lowering effect and stimulation of UKal by KCl supplementation and shows that variations in UKal correlate with urinary K and characterise patients with potassium sensitivity. Further studies, that include determinations of the circulating components of the kallikrein-kinin system, are required to elucidate whether bradykinin, the enzymatic product of kallikrein and potent stimulator of endothelial protective factors, may be a mediator of the vascular effects described for a high K intake.