Hitoshi Kontani*, Toshitsugu Tsuji and Satoko Kimura
Department of Pharmacology, Faculty of Pharmaceutical Science, Hokuriku University, Kanagawa-machi, Kanazawa 920-1181, Japan
*Corresponding author. FAX:+81-76-229-2781
Abstract: We investigated the effects of the adrenergic a2-receptor agonists clonidine, oxymetazoline and tizanidine on bladder contractions induced by infusing fluid into the bladders of conscious male rats. I.v. clonidine and oxymetazoline (both 0.01 to 0.1 mg/kg) caused bladder hyperactivity, expressed by shortening of the intercontraction interval. Tizanidine (0.1 mg/kg, i.v.) caused slight shortening of the intercontraction interval. The rank order of potency was clonidine = oxymetazoline >> tizanidine. Intrathecal (i.t.) injection of 10 mg clonidine and oxymetazoline, and intracerebroventricular (i.c.v) injection at 15 mg, produced almost the same pattern of bladder hyperactivity as that observed after i.v. injection of these drugs (0.03 mg/kg, i.v.). For all three administration routes of clonidine and oxymetazoline, i.v. idazoxan (0.3 mg/kg) exerted an inhibitory effect on the bladder hyperactivity induced by these drugs, except i.c.v injection of oxymetazoline. I.t. phenylephrine (30 mg) did not change the intercontraction interval. Although i.c.v. phenylephrine (15 mg) shortened the intercontraction interval, the potency was weaker than those of i.c.v. clonidine and oxymetazoline (15 mg). These results suggest that clonidine and oxymetazoline cause bladder hyperactivity by acting at adrenergic a2 receptors in the micturition centers of the lumbosacral and supraspinal regions.
Keywords: Rat micturition reflex, Bladder hyperactivity, Clonidine, Oxymetazoline,
Adrenergic a2-receptor agonist
Copyright© The Japanese Pharmacological Society 2000
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