Effect of testosterone replacement or duration of castration on baroreflex bradycardia in conscious rats.
BACKGROUND
In this study, we tested the hypothesis that 17beta-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.


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


CONCLUSIONS
The data suggest: 1) 17beta-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.
Ward
Gregg R
GR
Department of Pharmacology, The Brody School of Medicine at East Carolina University, Greenville, NC, 27858, USA.
Abdel-Rahman
Abdel A
AA
Department of Pharmacology, The Brody School of Medicine at East Carolina University, Greenville, NC, 27858, USA.
D000818:Animals; D017704:Baroreflex / Q000187:drug effects* / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D001919:Bradycardia / Q000209:etiology*; D004958:Estradiol / Q000494:pharmacology; D008297:Male; D009919:Orchiectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D013739:Testosterone / Q000097:blood / Q000494:pharmacology / Q000502:physiology*; D013997:Time Factors
D013739:Testosterone; D004958:Estradiol