Effects of sex hormones on development of physiological and pathological cardiac hypertrophy in male and female rats.

Previous studies have demonstrated a role for sex hormones in maintaining normal heart weight and myosin isoenzyme balance in the rat. To determine if sex hormones were necessary to elicit cardiac adaptations to the chronic loads of swimming or hypertension, female rats were gonadectomized (X) and then exposed either to a chronic swimming program (Sw) or to renal hypertension for 8-10 wk. Because gonadectomy in females increased heart and body weight, separate groups of food-restricted sedentary and Sw gonadectomized females (XFR) were included. Swimming resulted in significant increases in both heart weight and in the percent ventricular V1 isomyosin in female controls (C), X, and XFR. Hypertension was studied in C, X, and X with estrogen replacement. Cardiac hypertrophy developed in all groups, but estrogen therapy attenuated the decline in percent V1 isomyosin in both normotensive and hypertensive X animals. Swimming, which is generally not associated with cardiac hypertrophy in males, was also studied in that sex. Gonadectomy did not alter either the heart weight or the myosin isoenzyme response to Sw, although testosterone replacement in gonadectomized males restored ventricular V1 myosin levels to or above normal. Measures of serum thyroid levels and of myocardial catecholamines failed to demonstrate a causal relationship between these hormones and the various results. Therefore, although sex hormones are important for maintaining normal heart weights and myosin isoenzyme balance in rats, they do not appear to be important in the adaptations hearts exhibit when exposed to physiological or pathological loads.