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.
D000450:Aldosterone / Q000097:blood; D005665:Furosemide / Q000627:therapeutic use*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007610:Kallikreins / Q000502:physiology*; D007668:Kidney / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D011187:Posture; D012039:Regional Blood Flow / Q000187:drug effects; D012083:Renin / Q000097:blood
D000450:Aldosterone; D005665:Furosemide; D007610:Kallikreins; D012083:Renin