Androgen receptors mediate hypertrophy in cardiac myocytes

• Published in: Circulation (New York, N.Y.) Vol. 98; no. 3; pp. 256 - 261
• Main Authors: MARSH, J. D, LEHMANN, M. H, RITCHIE, R. H, GWATHMEY, J. K, GREEN, G. E, SCHIEBINGER, R. J
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 21.07.1998; American Heart Association, Inc
• Subjects: Adult; Animals; Biological and medical sciences; Cardiology. Vascular system; Cardiomegaly - etiology; Cells, Cultured; Dogs; Female; Heart; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Humans; Infant; Male; Medical sciences; Myocardium - metabolism; Myocardium - pathology; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; Receptors, Androgen - genetics; Receptors, Androgen - physiology; RNA, Messenger - metabolism; Signal Transduction - physiology; Transcription, Genetic; Heart; Human; Androgen; Pathophysiology; Heart disease; Cardiovascular disease; Exploration; Sex steroid hormone; Hypertrophy; Myocyte; Hormonal receptor
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.98.3.256

The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain. Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response. We used reverse transcription-polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [3H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion. Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.