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-1) was used to assess baroreflex bradycardia.ResultsAndrogen 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 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-1) of flutamide. 3) The absence of a change in serum 17β-estradiol rules out its contribution to flutamide action on baroreflex bradycardia.
Highlights
Previous studies have shown that testosterone enhances 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
The baroreflex bradycardia was significantly reduced compared with the sham-operated rats (1.23 ± 0.11 vs. -1.84 ± 0.24 beats min-1 mmHg-1; Figure 2)
Summary
Conscious unrestrained rats were used to investigate the role of the androgen receptor in the testosterone-mediated modulation of baroreflex bradycardia. Our preliminary findings [1], confirmed later by El-Mas et al [2], have provided evidence that androgens (including testosterone) play an important role in the mediation of baroreflex bradycardia. The effect of androgens on baroreflex bradycardia has been previously reported, no studies have investigated the possible involvement of the androgen receptor in mediating the effect of testosterone on baroreflex bradycardia. There are two actions that must be considered when flutamide is administered It leads to significant elevation in serum testosterone due to its ability to increase plasma levels of lutenizing hormone (LH) via preventing the activation of the testosterone-mediated negative feedback (page number not for citation purposes)
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