Natriuretic effect of acute nifedipine administration is not mediated by the renal kallikrein-kinin system.
J Cardiovasc Pharmacol
; 9(5): 536-40, 1987 May.
Article
em En
| MEDLINE
| ID: mdl-2439833
ABSTRACT
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Calicreínas
/
Nifedipino
/
Rim
/
Cininas
/
Natriurese
Tipo de estudo:
Clinical_trials
Limite:
Adult
/
Humans
/
Male
Idioma:
En
Revista:
J Cardiovasc Pharmacol
Ano de publicação:
1987
Tipo de documento:
Article