• AT1receptor;
  • renin-angiotensin system;
  • androgen;
  • epididymis

Our previous studies have provided solid evidence for the presence of an intrinsic angiotensin-generating system in the rat epididymis, which plays an important role in the regulation of the anion and thus fluid secretion by the epididymal epithelium. In the present study, the effect of androgen on the expression of AT1receptor and its subsequent regulation of anion secretion by the epididymis were investigated using Western blotting, semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and in vitro electrophysiological approaches. Results from Western blotting analysis showed that the expression of AT1receptor protein was almost abolished by castration whereas its expression was completely restored to the control level when the castrated rats were hormonally replaced with testosterone. Efferent duct ligation, however, appeared not to affect the expression of AT1receptor protein by the epididymis. Results from RT-PCR showed that mRNA expression of AT1receptor was consistent with that observed in protein expression. Results from short-circuit current (ISC) showed that castration almost abolished the angiotensin II-induced ISC. However, efferent duct ligation did not affect the angiotensin II-induced ISC, which was completely blocked in the presence of losartan, a specific antagonist of the AT1receptor. These data indicate that the expression of epididymal AT1receptor is predominantly influenced by testicular androgens but not by testicular factors. This androgen-dependent expression of AT1receptor could have a role in the control of AT1receptor-mediated anion secretion and thus fluid secretion by the rat epididymis.