EVIDENCE FOR CENTRAL ALPHA_2-ADRENERGIC MECHANISM OF CLONIDINE-INDUCED EJACULATORY DISTURBANCE IN DOGS

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In order to clarify the central mechanism of clonidine (CL)-induced sexual dysfunction such as erectile and ejaculatory disturbances, we examined the effects of intracerebroventricularly (i.c.v.) administered CL on erection and ejaculation in male dogs. CL (0.5-5μg/kg) produced a dose-related inhibition of ejaculation but not significant inhibition of erection by the manual stimulation of the penis. Sperm was not found in the urine drawn from the urinary bladder, suggesting that the inhibitory effect of CL on ejaculation was not due to retrograde ejaculation. The ejaculatory disturbance elicited by CL (5μg/kg) was antagonized by an α_2-adrenoceptor antagonist, yohimbine (1-10μg/kg, i.c.v.) in a dose-related manner. In contrast to the effect of yohimbine, it was unaffected by an α_1-adrenoceptor antagonist, prazosin (3 and 10μg/kg, i.c.v.). These results indicate that i.c.v. administered CL may selectively inhibit the ejaculatory response, which is presumably mediated through the stimulation of α_2-adrenoceptors.
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