Effect of testosterone replacement or duration of castration on baroreflex bradycardia in conscious rats
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Date
2005-03-30
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Authors
Ward, Gregg R.
Abdel-Rahman, Abdel A.
Journal Title
Journal ISSN
Volume Title
Publisher
East Carolina University
Abstract
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)
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 2005
Description
Citation
BMC Pharmacology; 5:9 p. 1-6
DOI
10.1186/1471-2210-5-9