Testosterone facilitates the baroreceptor control of reflex bradycardia: Role of cardiac sympathetic and parasympathetic components

Reported clinical and experimental findings have shown that baroreflex cont rol of heart rate is attenuated in women compared with men. This study inve stigated whether the sexual dimorphism in baroreflex function relates to th e ability of the male hormone testosterone to facilitate baroreflex respons iveness. Relative contributions of the vagal and sympathetic autonomic comp onents to testosterone modulation of baroreflex function were also investig ated. Baroreflex curves relating changes in heart rate to increases or decr eases in blood pressure evoked by phenylephrine and sodium nitroprusside, r espectively, were constructed in sham-operated rats and castrated rats with and without testosterone replacement. Slope of the curves was taken as an index of baroreflex sensitivity (BRSPE and BRSNP). Castration (for 10 days) significantly reduced plasma testosterone levels and attenuated reflex bra dycardia, as indicated by significantly smaller BRSPE in castrated rats com pared with values in sham-operated rats (-0.85 +/- 0.07 vs. -1.51 +/- 0.10 beats/min per min Hg). Testosterone replacement in castrated rats restored plasma testosterone and BRSPE to levels similar to those of sham-operated r ats. Muscarinic blockade by atropine caused 55% reduction in BRSPE in sham- operated rats, an effect that was significantly (p < 0.05) attenuated in ca strated rats and restored to intact levels after testosterone supplementati on, beta -Adrenergic blockade by propranolol caused slight and insignifican t decreases in BRSPE Castration and testosterone supplementation had no eff ect on BRSNP, ruling out a modulatory effect of testosterone on reflex tach ycardia. These data provide the first experimental evidence of a favorable role for testosterone in baroreceptor control of reflex bradycardia. Furthe r, baroreflex modulation by testosterone appears to be autonomically mediat ed and involves an enhancement of cardiomotor vagal activity.