We have previously reported that intravenous (i.v.) administration and intracerebroventricular administration of clonidine, a lipophilic α2-adrenoceptor agonist, significantly inhibited colonic motility in rats, but did not inhibit colonic motility in vitro. This inhibitory effect was significantly antagonized by pre-administraion of yohimbine, an α2-adrenoceptor antagonist, but not by pre-administration of prazosin, an α1-adrenoceptor antagonist. We presume that the mechanism of the inhibitory effect of clonidine on the colonic motility might involve in an indirect action mediated by activation of α2-adrenoceptors at sites outside the colon. Since clonidine could cross the blood-brain barrier, it is unclear whether clonidine inhibits colonic motility through activation of central or peripheral α2-adrenoceptors. The aim of this study was to investigate the site of α2-adrenoceptors involved in the inhibitory effect on colonic motility in rats. The hydrophilic α2-adrenoceptor agonist apraclonidine which could not easily cross the blood-brain barrier was used. Intravenous administration of apraclonidine was found to suppress the colonic motility with a dose-dependent manner. The inhibitory effect induced by apraclonidine (i.v.) on colonic motility was significantly antagonized by pre-administration of yohimbine. These results suggest that the suppression of colonic motility by α2-adrenoceptor agonist involves in activation of peripheral α2-adrenoceptors, but not at the site of colon. [Jpn J Physiol 54 Suppl:S200 (2004)]
