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

Abdel A Abdel-Rahman,Gregg R Ward

doi:10.1186/1471-2210-5-9

Abstract

BackgroundIn 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.ResultsTestosterone (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.ConclusionThe 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.

Highlights

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
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
This suggests that the long-term modulation of baroreflex sensitivity occurs independent of androgens, or the baroreflex mechanism may become adapted to low levels of circulating androgen

Summary

Introduction

We tested the hypothesis that 17β-estradiol contributes to testosterone-mediated restoration of baroreflex-mediated bradycardia in short-term (3 weeks) castrated rats. Factors influencing baroreflex sensitivity include gender, age, baseline mean arterial pressure and heart rate, anesthesia, and the method of drug administration [3-9] These factors cannot account for the difference in baroreflex sensitivity between intact and castrated rats in reported studies [1,2]. Ando et al [12] demonstrated a reflex increase in circulating testosterone of adrenocortical origin subsequent to long-term (6 weeks) castration The impact of such an increase in serum testosterone on baroreflex sensitivity is not known. The main objective of this study was to test the hypotheses that (i) 17β-estradiol, contributes to testosterone restoration of the vagal component of baroreflex sensitivity in shortterm (3 weeks) castrated rats, and (ii) the spontaneous increase in serum testosterone, or androstenedione,

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