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 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.

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; Rubattu, Speranza Donatella; C., Troffa; G. C., Tonolo. - In: JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. - ISSN 0160-2446. - 9:5(1987), pp. 536-540. [10.1097/00005344-198705000-00005]

NATRIURETIC EFFECT OF ACUTE NIFEDIPINE ADMINISTRATION IS NOT MEDIATED BY THE RENAL KALLIKREIN-KININ SYSTEM

RUBATTU, Speranza Donatella;
1987

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 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 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.
1987
01 Pubblicazione su rivista::01a Articolo in rivista
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; Rubattu, Speranza Donatella; C., Troffa; G. C., Tonolo. - In: JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. - ISSN 0160-2446. - 9:5(1987), pp. 536-540. [10.1097/00005344-198705000-00005]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/423297
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