Effect of low androgen status on the expression of adenosine A _2A and A _2B receptors in rat penile corpus cavernosum

Abstract

To investigate whether low androgen status affects erectile function by regulating the expression of adenosine A2A and A2B receptors in rat penile corpus cavernosum. Thirty‐six 8‐week‐old male Sprague‐Dawley rats were randomly divided into six groups: sham‐operated group (4w‐sham, 8w‐sham), castration group (4w‐cast, 8w‐cast) and androgen replacement group (4w‐cast+T, 8w‐cast+T). The rats in the androgen replacement groups were subcutaneously injected with testosterone propionate (3 mg/kg) every other day after castration. The maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP), the expression of A2A, A2B, AKT and eNOS and the concentrations of cAMP and cGMP in the corpus cavernosum were detected at the 4th and 8th weeks after the operation. The serum testosterone level and the ratio of ICPmax/MAP decreased significantly in the castration group as compared to other groups (p < 0.01). There was no significant difference in the expression of A2A receptor among groups, while the expression of A2B, AKT and eNOS and the concentrations of cAMP and cGMP in the castration group were significantly lower than in other groups (p < 0.01). Low androgen status inhibits the AKT/eNOS/cGMP signalling pathways and the production of cAMP in the corpus cavernosum of castrated rats by down‐regulating the expression of A2B receptor, and results in decreased of ICPmax/MAP.

Low androgen level impairs erectile function of rat by regulating the Ng/CaN/AKT/eNOS pathway in penile corpus cavernosum

“…Meanwhile, compared to the control group and castrated+T replacement group, the concentration of NO in the penile cavernous tissue of rat was remarkably decreased in the castrated group. These results indicated that the low androgen level inhibiting the production of NO in the penile carvernous tissue of rat and impaired erectile function; it was consistent with our previous study 22,23 …”

“…This may result in producing and maintaining penile erection. Our previous study confirmed that inhibition of the AKT/eNOS pathway is one of the molecular mechanisms by which low androgen level impaired erectile function, 25 which was the result of down‐regulating the d level of A2b receptors in penile cavernous tissue of rat with low androgen level 23 . Furthermore, this study found that compared to the control group and castrated+T replacement group, p‐eNOS/eNOS and p‐AKT/AKT in penile cavernous tissue of rat were remarkably decreased in the castrated group.…”

“…These results indicated that the low androgen level inhibiting the production of NO in the penile carvernous tissue of rat and impaired erectile function; it was consistent with our previous study. 22,23 This study found that Ng and CaN were primarily expressed in the cell cytoplasm and membrane of endothelial cells in rat penile cavernous tissue, and they are also found to be expressed in smooth muscle cells. Compared to the control group and castrated+T replacement group, the level of Ng in penile cavernous tissue of rat was remarkably decreased in the castrated group.…”

“…Based on our previous method, 22,23 4 weeks and 8 weeks after castration and testosterone replacement therapy, MAP and ICPmax were monitored in rats following anesthesia with 1% sodium pentobarbital.…”

“…Based on our previous method, 22,23 the penile cavernous tissue of rat was sectioned and then deparaffinized with xylene and gradient alcohol. Then add 3% hydrogen peroxide to remove endogenous catalyses, add citrate buffer for microwave antigen retrieval, and add BSA blocking solution to block nonspecific sites.…”