Alpha1-adrenoceptors in testosterone-induced prostatic hypertrophy.

Modifications of rat prostatic alpha1-adrenoceptors were investigated in testosterone-induced prostatic hypertrophy. [3H]prazosin bound to a single class of binding sites with a dissociation constant of 57.9+/-5.02 pM. The greater part of the binding capacity (24.6+/-1.02 fmol/mg protein) was made up of chloroethylclonidine-resistant binding sites that showed high-affinity for oxymetazoline and 5-methyl-urapidil, and was identified as alpha1A-adrenoceptors. The remaining chloroethylclonidine-sensitive binding sites that showed low-affinity for oxymetazoline and 5-methyl-urapidil were preferentially identified as alpha1B-adrenoceptors. mRNA for the three alpha1-adrenoceptors (alpha1a, alpha1b and alpha1d) was detected. Testosterone administration produced a 23% decrease of alpha1-adrenoceptor density, likely by an increase of prostatic glandular epithelium and a decrease in the relative proportion of smooth muscle, thus of alpha1-adrenoceptor density. The steady state level of mRNAs for alpha1-adrenoceptors was not modified by testosterone treatment. These results indicate that prostate alpha1-adrenoceptors are not affected in the prostatic hypertrophy induced by testosterone.