Orchiectomy or androgen receptor blockade attenuates baroreflex-mediated bradycardia in conscious rats

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 microg 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 17beta-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 17beta-estradiol rules out its contribution to flutamide action on baroreflex bradycardia.