Why the study?
Does testosterone replacement restore baroreflex-mediated bradycardia in castrated rats?
Does testosterone replacement restore baroreflex-mediated bradycardia in castrated rats?
Testosterone restores baroreflex-mediated bradycardia in short-term castrated rats independent of 17beta-estradiol, while long-term castration leads to spontaneous recovery of the reflex despite suppressed androgens.
Testosterone may modulate baroreflex sensitivity in short-term hypogonadism models; leaves open translation to human autonomic or cardiovascular outcomes.
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.
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Ward et al. (2005) studied this question.
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