Involvement of kallikrein in the antihypertensive response to furosemide in essential hypertension.

Twelve white men with essential hypertension were treated for 1 month in randomized order with either placebo or low-dose furosemide (40 mg/day) and compared to 22 race-, age-, and diet-matched normal controls. Furosemide therapy significantly reduced mean arterial pressure (108.6 +/- 2.4 vs. 101.0 +/- 2.7 mm Hg, p < 0.02) in association with a significant increase in 24 hr urinary kallikrein activity (7.9 +/- 1.8 vs. 13.4 +/- 2.8 esterase units/24 hr, p < 0.02). Normal controls on no therapy excreted 19.4 +/- 2.6 esterase units/24 hr of urinary kallikrein activity, significantly greater than hypertensives on placebo (p < 0.01) but not hypertensives on furosemide (p > 0.1). A significant (p < 0.05) inverse correlation between mean arterial pressure and urinary kallikrein activity suggests a possible role for the kallikrein-kinin system in the antihypertensive mechanism of furosemide.