Natriuretic effect of acute nifedipine administration is not mediated by the renal kallikrein-kinin system

P. Madeddu, M. Oppes, A. Soro, P. Dessi’-Fulgheri, N. Glorioso, F. Bandiera, P. Manunta, S. Rubattu, C. Troffa, G. C. Tonolo, G. F. Cocco, A. Rappelli

Research output: Contribution to journalArticlepeer-review


Despite their vasodilating action, calcium antagonists increase renal sodium excretion. To ascertain whether renal kallikrein plays a role in the renal effects of calcium antagonists, nifedipine (N) (10 mg orally) or placebo (P) was given to 17 male patients with mild to moderate essential hypertension during a 6-h infusion of either saline (S) or aprotinin (A) (2 x 106 KIU in 200 ml of saline). Blood pressure (BP) and heart rate (HR) were measured every 10 min, and blood samples were taken at - 10, 0, 30, 60, 120, 240, 360 min for plasma renin activity (PRA), creatinine, and osmolarity determinations. Urinary kallikrein, aldosterone, creatinine, and electrolytes were measured in 6-h urine collections. The acute administration of N induced a significant systolic BP (SBP) and diastolic (DBP) fall and a transient PRA increase that peaked at 30 min and were not modified by A infusion. Urinary volume (+47%), Na+ (+54%) and C1- (+58%) excretion were significantly enhanced by N. There were less pronounced and statistically not significant increases in urinary excretion of Ca2+ (+38%) and K+ (+29%). Infusion of A did not interfere with the natriuretic effect of N. Our data do not support the hypothesis that the kallikrein-kinin system plays an important role in mediating the renal effects of nifedipine in humans.

Original languageEnglish
Pages (from-to)536-540
Number of pages5
JournalJournal of Cardiovascular Pharmacology
Issue number5
Publication statusPublished - 1987


  • Calcium antagonist
  • Kallikrein
  • kinin system
  • Nifedipine

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology


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