Effect of testosterone replacement or duration of castration on baroreflex bradycardia in conscious rats

Background: In this study we tested the hypothesis that 17β-estradiol contributes to testosterone-mediated restoration of baroreflex-mediated bradycardia in short-term (3 weeks) castrated rats. Further a reported increase in serum testosterone after long-term (6 weeks) astration constituted a basis for testing the hypothesis that a spontaneous increase in serum testosterone or androstenedione in this model causes a commensurate increase in baroreflexmediated bradycardia. Results: Testosterone (1 week) replacement enhanced baroreflex-mediated bradycardia in shortterm castrated rats without changing 17β-estradiol level. A spontaneous recovery of baroreflexmediated bradycardia occurred following long-term castration although circulating testosterone and androstenedione remained suppressed. Conclusion: The data suggest: 1) 17β-Estradiol does not contribute to testosterone restoration of the baroreflex-mediated bradycardia in short-term castrated rats. 2) The long-term modulation of baroreflex-mediated bradycardia occurs independent of androgens or the baroreflex mechanism may become adapted to low levels of circulating androgens. Originally published BMC Pharmacology Vol. 5 No. 9 Mar 200