Dynamic aldosterone and 18-hydroxydeoxycorticosterone studies in labile and stable benign essential hypertension

Abstract

Under baseline conditions of recumbency and normal sodium intake there was a small significant hyperaldosteronism evident from elevated plasma concentration and aldosterone excretion in presence of suppressed metabolic clearance rate (MCR) in benign essential hypertension (BEH). BEH patients, particularly those with hyperkinetic circulation often excreted more oxo-conjugate and present greater than normal response in plasma aldosterone to upright posture. Upright posture decreased aldosterone MCR in controls, but effect was negligible in BEH. In BEH, decreased MCR and excretion of hepatic metabolite (tetrahydroaldosterone) may be due to impaired hepatic extraction related to increased aldosterone binding to a transcortin-like plasma fraction (TLPF). Concomitant fluctuations of TLPF and plasma concentration during circadian rhythm, the menstrual cycle and pregnancy suggest a possible role of TLPF in aldosterone distribution and dynamics. Recumbent BEH patients had increased plasma aldosterone around midnight. BEH patients showed hyperresponsiveness to ACTH infusion in plasma aldosterone with simultaneous sharp decrease of TLPF binding, while aldosterone MCR increased significantly and the ratio of the urinary and hepatic metabolites of aldosterone changed. Changes in binding degree probably contribute to perturbated aldosterone metabolism in BEH. In the majority of BEH patients with normal or low plasma renin activity 18-hydroxydeoxycorticosterone secretion is increased. ACTH stimulation or dexamethasone suppression of 18-hydroxydeoxycorticosterone is comparable in controls and patients. This hormone circulates in unbound form.