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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 2 611-615
Copyright © 1997 by The Endocrine Society

Endocrinological Oncology

Somatic Mutations of the Angiotensin II (AT1) Receptor Gene are Not Present in Aldosterone-Producing Adenoma1

Eleanor Davies2, Alain Bonnardeaux, Pierre-François Plouin, Pierre Corvol and Eric Clauser

INSERM U-36, Collège de France, Paris, France

Address all correspondence and requests for reprints to: Dr. Eric Clauser, INSERM U-36, Collège de France, 3 rue d’Ulm, 75005 Paris, France.

Angiotensin II stimulates aldosterone secretion from the adrenal zona glomerulosa and mediates most of its biological effects via G protein-coupled type 1 angiotensin II receptors (AT1). A number of G protein-coupled receptors are constitutively activated as a result of somatic mutations in the gene encoding the protein. It is, therefore, possible that primary hyperaldosteronism caused by an aldosterone-producing adenoma (APA) may be the result of constitutive activation of the AT1 receptor. The 1.1-kilobase coding region (exon 5) of the AT1 receptor gene was analyzed in APA and normal adrenal tissue for the presence of mutations using single stranded conformational polymorphism and sequencing techniques. In 17 APAs, no functional mutations were found that could account for the observed pathophysiology. However, three silent polymorphisms were detected in regions encoding the second extracellular loop, the intracellular arm preceding the COOH terminal, and the 3'-untranslated region. In conclusion, somatic mutations in the coding region of the AT1 receptor gene do not appear to play a role in primary hyperaldosteronism caused by an APA.




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