PMID: 8582487Nov 20, 1995Paper

Mechanism of inhibition of aldosterone secretion by a Ca2+ channel blocker in patients with essential hypertension and patients with primary aldosteronism

Nihon Naibunpi Gakkai zasshi
T YokoyamaO Iimura

Abstract

Three studies were conducted in order to investigate the suppressive effects of a calcium antagonist on aldosterone secretion and a possible mechanism. Study 1: A long-term (4 weeks) treatment with slow-release nifedipine (Nif), 40-60 mg/day, was performed in 9 in-patients with essential hypertension (EHT). Mean arterial pressure (MAP), plasma renin activity (PRA), plasma angiotensin II levels (pAII) and plasma aldosterone concentration (PAC) were determined before and after Nif treatment. Study 2: In another 7 in-patients with EHT, Nif treatment (40-60 mg, 7-10 days) was carried out to study its effect on aldosterone secretion in response to 2-hour ambulation, angiotensin II (AII) infusion (2.5 ng/kg/min, for 1-hour) and ACTH injection (2.5 mg i.v.). Study 3: The effects of Nif (40-60 mg/day, for 7-10 days) on MAP, PAC, serum potassium, potassium clearance (Ck) and changes in PAC or plasma cortisol levels in response to ACTH injection (2.5 mg i.v.) were studied in 6 in-patients with primary aldosteronism (PA). In patients with EHT, MAP was reduced significantly at 1 week and 4 weeks after the administration of Nif. PRA and pAII increased significantly, though the increase of PAC was not significant. In the low-renin EHT group,...Continue Reading

Citations

Mar 21, 2007·Hypertension Research : Official Journal of the Japanese Society of Hypertension·UNKNOWN Japanese Society of Hypertension

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