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Open Access Research article

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

Gregg R Ward and Abdel A Abdel-Rahman*

Author Affiliations

Department of Pharmacology, The Brody School of Medicine at East Carolina University, Greenville, NC, 27858, USA

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BMC Pharmacology 2005, 5:9  doi:10.1186/1471-2210-5-9

Published: 30 March 2005



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 baroreflex-mediated bradycardia.


Testosterone (1 week) replacement enhanced baroreflex-mediated bradycardia in short-term castrated rats without changing 17β-estradiol level. A spontaneous recovery of baroreflex-mediated bradycardia occurred following long-term castration, although circulating testosterone and androstenedione remained suppressed.


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.