Summary: 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/24hr of urinary kallikrein activity, significantly greater than hypertensives on placebo (p < 0.01) but not hypertensives on furosemide (p < 0.01). The decrease in mean arterial pressure and the increase in urinary kallikrein activity induced by furosemide were not associated with a demonstrable change in renal hemodynamics. plasma renin activity, or plasma aldosterone concentration, but they were associated with a significant increase in intravascular volume (5.876 ± 339 vs. 6.808 ± 346 ml. p < 0.01). 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.
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Olshan et al. (1981) studied this question.