Different effect of clonidine on 2-deoxy-D-glucose-stimulated gastric motor function after central or peripheral administration in anesthetised rat

Introduction: Our previous findings suggested that α2-adrenoceptors are involved in mucosal protective processes. Since gastric motility may influence gastric mucosal defense the question was raised how activation of α2-adrenoceptors may influence gastric motor function.

Method: Experiments were performed on male Wistar rats anesthetized by urethane (1.25mg/kg, intraperitoneal). Gastric motility was measured using a rubber balloon inserted into the stomach via mouth. Drugs were given intracerebroventricularly (icv.) or intravenously (iv.).

Results: 1. Clonidine (0.75–3.76 nmol/kg) after iv. administration inhibited both the increased gastric pressure and gastric contraction induced by deoxy-D-glucose (300mg/kg, iv.). The effect was reversed by yohimbine given iv. (4mg/kg, iv.), but not by icv. (50 nmol/rat) route of administration. 2. In contrast, clonidine injected icv. in the dose of 3,8–19 nmol/rat either failed to influence or slightly increased the intragastric pressure. The later effect was reversed by yohimbine given either icv. or iv. (50 nmol/rat, icv or 4mg/kg, iv.).

Conlcusion: Clonidine induces different effect on gastric motor function following peripheral or central administration in anesthetized rat. The peripheral inhibitory effect of clonidine may be due to activation presynaptic α2-adrenoceptors at cholinergic nerve terminal resulting in inhibition of ACh release. In contrast, clonidine following central administration might activate dorsal motor nucleus of vagus which would result in increased gastric motor activity.

The work was supported by grants OTKA T 032607 and ETT 389/2003.