Orchiectomy or androgen receptor blockade attenuates baroreflex-mediated bradycardia in conscious ratsReport as inadecuate




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BMC Pharmacology

, 6:2

First Online: 23 January 2006Received: 09 November 2004Accepted: 23 January 2006

Abstract

BackgroundPrevious studies have shown that testosterone enhances baroreflex bradycardia. Therefore, conscious unrestrained rats were used to investigate the role of the androgen receptor in the testosterone-mediated modulation of baroreflex bradycardia. Androgen depletion 3 weeks, and androgen receptor blockade 20–24 h, were implemented to test the hypothesis that testosterone influences baroreflex bradycardia via its activity at the androgen receptor in male rats. Phenylephrine 1–16 μg kg was used to assess baroreflex bradycardia.

ResultsAndrogen depletion attenuated baroreflex bradycardia P < 0.01. The antiandrogen flutamide 5, 15, or 30 mg kg, s.c. caused dose-related attenuation of baroreflex bradycardia in spite of a significant P < 0.05 increase in serum testosterone. The latter did not lead to increased serum 17β-estradiol level.

ConclusionThe data suggest: 1 Androgen depletion or adequate androgen receptor blockade attenuates baroreflex bradycardia. 2 The reflex increase in serum testosterone may counterbalance the action of the lower doses 5 or 15 mg kg of flutamide. 3 The absence of a change in serum 17β-estradiol rules out its contribution to flutamide action on baroreflex bradycardia.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2210-6-2 contains supplementary material, which is available to authorized users.

Gregg R Ward and Abdel A Abdel-Rahman contributed equally to this work.

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Author: Gregg R Ward - Abdel A Abdel-Rahman

Source: https://link.springer.com/



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