Gonadectomy and androgen replacement alter cardiac performance in conscious adult male rats.

Gender disparities in cardiac function have been described. Yet the extent to which gender related differences in cardiac performance are due to the presence of sex-specific biological factors are unclear. We used a longitudinal study aimed at examining whether castration and androgen replacement affects cardiac performance in conscious adult male rats. Adult male rats were implanted with Piezoelectric transit-time gauges and radio telemetry devices to measure regional myocardial segment length and hemodynamic variables before and after castration and after androgen replacement. Androgen withdrawal accelerated average heart rates by 7% (p=0.010). Heart rate was lowered to intact values when androgens were restored to normal physiological levels (p=0.004). Mean arterial pressure was not affected by androgen deprivation and androgen replacement. However, androgen withdrawal produced a 40% decrease in the velocity of circumferential shortening and a 46% reduction in the rate of myocardial relaxation. Androgen supplementation completely restored contractile function. These results provide the first evidence that androgen withdrawal and androgen replacement produces dramatic alterations on cardiac performance in conscious animals and demonstrates the significance of androgens as a cardio-regulatory hormone in males. Sex steroids are likely contributors to gender-related differences in cardiac function.

Daily exercise-induced cardioprotection is associated with changes in calcium regulatory proteins in hypertensive rats.

Epidemiological data document that regular exercise protects against the morbidity and mortality associated with ischemic heart disease. Therefore, we tested the hypothesis that daily exercise (DE) increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion and alters the expression of calcium regulatory proteins. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. To test this hypothesis, we recorded the VAT in conscious sedentary normotensive, sedentary hypertensive, and DE hypertensive rats, and we associated these thresholds with the protein expression of the L-type calcium channel, Na+/Ca2+ exchanger, phospholamban, and sarco(endo)plasmic reticulum Ca(2+)-ATPase. Results document a significantly reduced time to ventricular arrhythmias (sedentary hypertensive, 3.7 +/- 0.3 min vs. sedentary normotensive, 4.8 +/- 0.3 min), an increased Na+/Ca2+ exchanger protein expression (47%), and a decreased phospholamban protein expression (-34%) in conscious hypertensive rats. DE increased the VAT (5.9 +/- 0.2 min), decreased the protein expression of the Na+/Ca2+ exchanger, and normalized the protein expression of phospholamban in the hypertensive rats. Thus DE may be a primary prevention approach for reducing the incidence of arrhythmias by altering calcium regulatory proteins in hypertensive rats.