Sex-dependent effects of gonadal steroids and cortisol on cardiac contractility in rainbow trout

• Published in: Journal of experimental biology Vol. 207; no. Pt 12; pp. 2083 - 2093
• Main Authors: Farrar, Richard S, Rodnick, Kenneth J
• Format: Journal Article
• Language: English
• Published: England 01.05.2004
• Subjects: Analysis of Variance; Animals; Dose-Response Relationship, Drug; Estradiol - pharmacology; Female; Gonadal Steroid Hormones - pharmacology; Hydrocortisone - pharmacology; Male; Myocardial Contraction - drug effects; Nitric Oxide; Oncorhynchus mykiss - physiology; Polyamines; Sex Factors; Signal Transduction - drug effects; Testosterone - analogs & derivatives; Testosterone - pharmacology
• ISSN: 0022-0949; 1477-9145
• DOI: 10.1242/jeb.00996

The purpose of this study was to determine whether steroid hormones modulate cardiac function in rainbow trout (Oncorhynchus mykiss Walbaum). We assessed the effects of exogenously administered steroids on isolated ventricle strips and report that physiological concentrations of androgens, 17beta-estradiol and cortisol rapidly (<10 min) enhance inotropism (30-40%) in a sex-specific manner. These effects were specific to the hormones studied, absent if animals were anesthetized chemically and dependent upon steroid concentration and contraction frequency. Based on the use of specific steroid receptor antagonists and key enzyme inhibitors, it appears that testosterone, 11-ketotestosterone and cortisol each act through specific intracellular receptors in males and that the positive inotropism requires the synthesis of polyamines and nitric oxide. Cortisol and 17beta-estradiol, but not androgens, had similar effects in females and also involved similar signaling pathways. Androgen and cortisol effects were additive in males but cortisol and 17beta-estradiol were not additive in females, suggesting sex differences in the pathways through which these hormones stimulate inotropism. In summary, gonadal steroids and cortisol promote ventricular contractility in a sex-dependent manner through mechanisms that appear multifaceted. Ultimately, steroid-mediated improvements in cardiac performance might involve non-genomic pathways and be physiologically important during migration, spawning or stressful periods.