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

Abstract

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.

CONCLUSION:

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.

• Authors: Gregg R Ward, Abdel A Abdel-Rahman
• Journal: BMC pharmacology (BMC Pharmacol) Vol. 5 Pg. 9 (Mar 30 2005) ISSN: 1471-2210 [Electronic] England
• PMID: 15799780 (Publication Type: Journal Article)

Chemical References

• Testosterone
• Estradiol

Topics

• Animals
• Baroreflex (drug effects, physiology)
• Blood Pressure (drug effects)
• Bradycardia (etiology)
• Estradiol (pharmacology)
• Male
• Orchiectomy
• Rats
• Rats, Sprague-Dawley
• Testosterone (blood, pharmacology, physiology)
• Time Factors