Ward, Gregg R.Abdel-Rahman, Abdel A.2011-04-282011-05-172011-04-282011-05-172005-03-30BMC Pharmacology; 5:9 p. 1-6http://hdl.handle.net/10342/3435Background: 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) castration 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 2005en-USAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.Baroreflex bradycardiaTestosterone replacementCastration durationArticlePMC107988410.1186/1471-2210-5-9