Abstract
Background: Previous 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-1) was used to assess baroreflex bradycardia. Results: Androgen depletion attenuated baroreflex bradycardia (P < 0.01). The antiandrogen flutamide (5, 15, or 30 mg kg-1, 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 17ß-estradiol level. Conclusion: The 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-1) of flutamide. 3) The absence of a change in serum 17β-estradiol rules out its contribution to flutamide action on baroreflex bradycardia. © 2006 Ward and Abdel-Rahman; licensee BioMed Central Ltd.
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CITATION STYLE
Ward, G. R., & Abdel-Rahman, A. A. (2006). Orchiectomy or androgen receptor blockade attenuates baroreflex-mediated bradycardia in conscious rats. BMC Pharmacology, 6. https://doi.org/10.1186/1471-2210-6-2
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