Effects of castration on contraction and α1‐adrenoceptor expression in rat prostate

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Abstract
The prostate function is regulated by androgens and α‐adrenergic activity. Clinically, antiandrogens and/or α1‐adrenergic antagonists are commonly used to treat symptomatic prostatic hypertrophy. To elucidate the effects of androgen deprivation on prostate contractility via α1‐adrenoceptor, the characteristics and expression of α1‐adrenoceptors were examined in castrated rats. Isolated prostate strips from intact and castrated rats were subjected to a phenylephrine stimulated contraction. Prazosin (10 nM), [3H]‐prazosin and phenoxybenzamine (3–300 nM) were used for inhibition assay, receptor characterization and partial alkylation of α‐adrenoceptor, respectively. The mRNA content of three subtypes of α‐adrenoceptors was determined by reverse transcription combined with polymerase chain reaction (RT–PCR). Contractile response to phenylephrine increased in castrated rats, which could be explained by a relative increase of the stromal component. A lowered contraction potency was also noted in castrated rats. Receptor binding assay indicated minimal changes in the affinity or density of α1‐adrenoceptor. Escalating alkylation of the α1‐adrenoceptor population resulted in a rightward shift in the contraction‐response curves before depressing maximal contractile force, and the suppression was detected at lower doses in castrated rats. RT–PCR study confirmed the expression of three types of α1‐adrenoceptor, α1a, α1b and α1d‐adrenoceptors, in intact rat prostate, and revealed that α1a‐adrenoceptor, but not α1b or α1d‐adrenoceptors, was down‐regulated in castrates. The results show that androgen deprivation suppressed α1‐adrenergic contractility of rat prostate strips, and the suppression was associated with down‐regulation of receptor reserve for the α1a‐adreneroceptor population expressed in intact rat prostate. British Journal of Pharmacology (2000) 131, 1454–1460; doi:10.1038/sj.bjp.0703706

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