Hitoshi Kontani*, Toshitsugu Tsuji and Satoko Kimura
Department of Pharmacology, Faculty of Pharmaceutical Science, Hokuriku
University, Kanagawa-machi, Kanazawa 920-1181, Japan
*Corresponding author.ﾊﾊFAX:+81-76-229-2781
E-mail: h-kontani@hokuriku-u.ac.jp
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ﾊmg/kg) caused bladder hyperactivity,
expressed by shortening of the intercontraction interval. Tizanidine (0.1ﾊmg/kg,
i.v.) caused slight shortening of the intercontraction interval. The rank
order of potency was clonidineﾊ=ﾊoxymetazolineﾊﾊ>>ﾊtizanidine.
Intrathecal (i.t.) injection of 10ﾊmg clonidine
and oxymetazoline, and intracerebroventricular (i.c.v) injection at 15ﾊmg,
produced almost the same pattern of bladder hyperactivity as that observed
after i.v. injection of these drugs (0.03ﾊmg/kg, i.v.). For all three administration
routes of clonidine and oxymetazoline, i.v. idazoxan (0.3ﾊ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ﾊmg)
did not change the intercontraction interval. Although i.c.v. phenylephrine
(15ﾊmg) shortened the intercontraction interval,
the potency was weaker than those of i.c.v. clonidine and oxymetazoline
(15ﾊ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ｩ The Japanese Pharmacological Society 2000
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