[Effect of a calcium inhibitor, nicardipine, on aldosterone secretion in primary hyperaldosteronism].
The purpose of the study was to evaluate the effects of a dihydropyridine calcium antagonist, nicardipine (N), on blood pressure (BP) and aldosterone secretion in hypertensive patients (pt) with primary aldosteronism. The study concerned 8 pts, mean age 55.6 +/- 7.7 years, 1 pt with aldosterone-producing adenoma (APA) and 7 pts with idiopathic aldosteronism: plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were respectively 0.30 +/- 0.2 ng/ml/h) and 314 +/- 109 pg/ml. Acute administration of 12 mg of nicardipine during 90 mn (three periods of N infusion during 30 mn: 0.4 mg/mn-5 mn; then 0.08 mg/mn-25 mn) significantly decreased BP, with an increase in heart rate (HR); the levels of PAC were significantly reduced with a slight but not significant increase in PRA, 60 mn after N: (table; see text) N decreased also PAC in the pt with APA [600 to 410 pg/ml] but did not improve hypokalemia (3.1 vs 3.3 mmol/l, n = 8 N.S.). In contrast, PAC levels were not modified 2 hours after acute oral administration of captopril (1 mg/kg): 302 +/- 164 pg/ml vs 332 +/- 191 pg/ml (NS). This study demonstrated the antihypertensive efficacy of acute infusion of nicardipine in primary aldosteronism; the decrease of PAC under this calcium antagonist suggested its potential interest in the management of idiopathic aldosteronism.
Chamontin
B
B
Service de médecine interne, hôpital Purpan, Toulouse.
Begasse
F
F
David
D
D
Salvador
M
M
D000368:Aged; D000450:Aldosterone / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D002986:Clinical Trials as Topic; D004341:Drug Evaluation; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000378:metabolism*; D006973:Hypertension / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009529:Nicardipine / Q000494:pharmacology* / Q000627:therapeutic use
D000450:Aldosterone; D009529:Nicardipine
Effet d'un inhibiteur calcique, la nicardipine, sur la sécrétion de l'aldostérone au cours de l'hyperaldostéronisme primaire.