Properties of Alpha-1-Adrenergic Receptors in the Rat Prostate: Effect of Experimental Diabetes

We studied the effects of 8 weeks of streptozotocin (STZ)-induced diabetes on the density and the pharmacological properties of α 1 -adrenoceptors in the rat prostate using receptor-binding experiments with [ 125 I]iodo-2[β-(4-hydroxyphenyl)-ethylaminomethyl]tetralone [ 125 I]HEAT. Saturation experiments showed the presence of specific [ 125 I]HEAT-binding sites in the control and diabetic rat prostate and that the induction of diabetes significantly decreased the density of [ 125 I]HEAT-binding sites in the rat prostate. [ 125 I]HEAT-binding sites in the prostate of both groups were inhibited by prazosin (nonselective), spiperone (α 1B -selective), WB4101 and 5-methylurapidil (α 1A -selective) and BMY7378 (α 1D -selective) with the following rank order of K i values: prazosin < WB4101 < 5-methylurapidil < spiperone < BMY7378, indicating a similar pharmacological profile of α 1 -adrenoceptor in the 2 groups.Comparing the K i values of the rat prostate with those obtained from the rat submaxillary gland (α 1A ), rat spleen (α 1B ), rat vas deferens (α 1A + α 1B ) and those reported for cloned α 1D , indicates the predominance of the α 1A + α 1B or the α 1A subtype in the rat prostate. The present study demonstrates that STZ-induced diabetes downregulates the expression of α 1 -adrenoceptor in the rat prostate, without significantly affecting the receptor subtype specificity.