Ward, Gregg R.Abdel-Rahman, Abdel A.2011-04-282011-05-172011-04-282011-05-172006-01BMC Pharmacology; 6:2 p. 1-8http://hdl.handle.net/10342/3396Background: 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 17ß-estradiol rules out its contribution to flutamide action on baroreflex bradycardia. Originally published BMC Pharmacology, Vol. 6, No. 2, Jan 2006en-USAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.Baroreflex bradycardiaAndrogen receptorArticlePMC140375910.1186/1471-2210-6-2