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Evidence for a Role of Vasopressin in the Control of Aldosterone Secretion in Primary Aldosteronism: in Vitro and in Vivo Studies

Institut National de la Santé et de la Recherche Médicale Unité 413 (V.P., C.D., H.L., J.-L.D.R., H.V., J.-M.K.), Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France; and Institut National de la Santé et de la Recherche Médicale Center for Clinical Investigation 204 (H.L., J.-M.K.), University Hospital of Rouen, 76031 Rouen, France

Address all correspondence and requests for reprints to: Dr. Hubert Vaudry, Institut National de la Santé et de la Recherche Médicale Unité 413, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (Institut Fédératif de Recherche Multidisciplinaires sur les Peptides 23), University of Rouen, 76821 Mont-Saint-Aignan, France. E-mail: hubert.vaudry{at}univ-rouen.fr.

Context: Arginine vasopressin (AVP) stimulates steroid secretion from the normal human adrenal gland and some cortisol-producing adrenocortical tumors or hyperplasia through activation of the V_1a receptor.

Objective: The objective of the study was to investigate in vitro and in vivo the possible involvement of AVP in the physiopathology of primary aldosteronism.

Design: The design of the study included immunohistochemical, pharmacological, and molecular studies on aldosterone-producing adenoma (APA), followed by a monocentric, crossover trial of the orally active V_1a receptor antagonist, SR 49059, in a double blind, randomized, and placebo-controlled fashion.

Setting: The study was conducted at a university hospital and research laboratory.

Patients: The study population included eight untreated patients with primary aldosteronism, four with APA and four with idiopathic hyperaldosteronism.

Main Outcome Measures: Aldosterone secretion of APA cells in vitro and plasma aldosterone, renin, and ACTH were measured.

Intervention: SR 49059 (200 mg once daily) or placebo was administered during two 1-wk treatment periods separated by a 2-wk washout.

Results: We observed the occurrence of AVP-containing cells in APA tissues. Administration of AVP to perifused APA cells induced an increase in aldosterone production, which was inhibited by a specific V_1a antagonist. RT-PCR analysis showed the expression of V_1a receptor mRNA in most APAs studied. In APA patients, SR 49059 did not induce any effect on basal aldosterone secretion but provoked a plasma aldosterone response to orthostatism (P < 0.03) and strengthened the positive correlation between plasma aldosterone and ACTH.

Conclusions: The present study indicates that functional V_1a receptors are present in APA and suggests that AVP may exert an autocrine/paracrine control of aldosterone secretion in APA tissues.

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