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

A. R. Olshan, D. T. O'Connor, Richard A Preston, R. P. Frigon, R. A. Stone

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Abstract

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). 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.

Original languageEnglish
Pages (from-to)161-167
Number of pages7
JournalJournal of Cardiovascular Pharmacology
Volume3
Issue number1
StatePublished - Feb 9 1981
Externally publishedYes

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ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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