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