We studied the effects of 8 weeks of streptozotocin (STZ)-induced diabetes on the density and the pharmacological properties of alpha1-adrenoceptors in the rat prostate using receptor-binding experiments with [125I]iodo-2[beta-(4-hydroxyphenyl)-ethylaminomethyl]tetralone [125I]HEAT. Saturation experiments showed the presence of specific [125I]HEAT-binding sites in the control and diabetic rat prostate and that the induction of diabetes significantly decreased the density of [125I]HEAT-binding sites in the rat prostate. [125I]HEAT-binding sites in the prostate of both groups were inhibited by prazosin (nonselective), spiperone (alpha1B-selective), WB4101 and 5-methylurapidil (alpha1A-selective) and BMY7378 (alpha1D-selective) with the following rank order of Ki values: prazosin < WB4101 < 5-methylurapidil < spiperone < BMY7378, indicating a similar pharmacological profile of alpha1-adrenoceptor in the 2 groups. Comparing the Ki values of the rat prostate with those obtained from the rat submaxillary gland (alpha1A), rat spleen (alpha1B), rat vas deferens (alpha1A + alpha1B) and those reported for cloned alpha1D, indicates the predominance of the alpha1A + alpha1B or the alpha1A subtype in the rat prostate. The present study demonstrates that STZ-induced diabetes downregulates the expression of alpha1-adrenoceptor in the rat prostate, without significantly affecting the receptor subtype specificity.
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Nishi et al. (1998) studied this question.
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