Natriuretic effect of acute nifedipine administration is not mediated by the renal kallikrein-kinin system.
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 10(6) 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 Cl- (+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.
D000328:Adult; D000450:Aldosterone / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects; D004573:Electrolytes / Q000652:urine; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007610:Kallikreins / Q000502:physiology* / Q000652:urine; D007668:Kidney / Q000378:metabolism*; D007705:Kinins / Q000502:physiology*; D008297:Male; D009318:Natriuresis / Q000187:drug effects*; D009543:Nifedipine / Q000494:pharmacology*; D012083:Renin / Q000097:blood
D004573:Electrolytes; D007705:Kinins; D000450:Aldosterone; D007610:Kallikreins; D012083:Renin; D009543:Nifedipine