Loss of the Effects of Clonidine on the Growth Hormone Release and Hypotensive Action in Long-Term Castrated Rats: The Possible Role of Testosterone on Alpha-2-Adrenergic Mechanisms of Clonidine

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Abstract
The effect of testosterone on the growth hormone (GH)-releasing and hypotensive actions of clonidine was evaluated in vivo using male Wistar rats. Clonidine at various doses and by various routes (5 µg/kg, Lev.; 15 µg/kg, i.v., and 7, 15, 31, 125 and 250 µg/kg, i.p.) induced a significant increase in plasma GH levels in rats. Intracerebroventricular (5 µg/kg) injection of clonidine significantly decreased blood pressure. The effects of clonidine on the GH release and blood pressure were lost in long-term castrated rats, but were restored by testosterone replacement in the castrates. In addition, the hypotensive response to clonidine in testosterone-replaced castrated rats lasted longer than in the sham-operated rats. The injection of yohimbine (3 mg/kg, i.p.) strongly inhibited the secretion of GH induced by clonidine treatment in sham-operated animals, and its inhibitory action was significantly attenuated in castrates. In long-term castrated rats, basal blood pressure decreased significantly compared with that of sham-operated rats. This was also restored after testosterone administration to castrates. The results of the present study indicate that the α2-adrenergic receptor-mediated effects of clonidine on the GH release and blood pressure might be dependent on the endogenous testosterone secretion.