α1-Adrenoceptors in testosterone-induced prostatic hypertrophy

Modifications of rat prostatic alpha(1)-adrenoceptors were investigated in testosterone-induced prostatic hypertrophy. [H-3]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 low-affinity for oxymetazoline and 5-methyl-urapidil were preferentially identified as alpha(1B)-adrenoceptors. mRNA for the three alpha(1)-adrenoceptors (alpha(1A), alpha(1b) and alpha(1d)) was detected. Testosterone administration produced a 23% decrease of alpha(1)-adrenoceptor density, likely by an increase of prostatic glandular epithelium and a decrease in the relative proportion of smooth muscle, thus of alpha(1)-adrenoceptor density. The steady state level of mRNAs for alpha(1)-adrenoceptors was not modified by testosterone treatment. These results indicate that prostate alpha(1)-adrenoceptors are not affected in the prostatic hypertrophy induced by testosterone. (C) 1998 Elsevier Science B.V.