Characterisation of α 2-adrenoceptor subtypes involved in gastric emptying, gastric motility and gastric mucosal defence

Abstract

The effect of clonidine on ethanol-induced gastric mucosal damage, gastric emptying and gastric motility was compared. The clonidine-induced gastroprotective effect (0.03–0.09 μmol/kg, s.c.) was antagonised by yohimbine (5 μmol/kg, s.c.), prazosin (0.23 μmol/kg; α 2B-adrenoceptor antagonist) and naloxone (1.3 μmol/kg, s.c.). Clonidine also inhibited the gastric emptying of liquid meal (0.75–3.75 μmol/kg, s.c.) and gastric motor activity (0.75 μmol/kg, i.v.) stimulated by 2-deoxy- d-glucose (300 mg/kg, i.v.). Inhibition of gastric emptying and motility was reversed by yohimbine (5 and 10 μmol/kg, s.c., respectively), but not by prazosin (0.23 μmol/kg, s.c.) or naloxone (1.3 μmol/kg, s.c.). Oxymetazoline–an α 2A-adrenoceptor agonist–inhibited both gastric emptying (0.67–6.8 μmol/kg, s.c.) and motility (0.185–3.4 μmol/kg, i.v.), whereas it failed to affect gastric mucosal lesions. The results indicate that in contrast to the gastroprotective effect, which is mediated by α 2B-adrenoceptor subtype, α 2A-adrenoceptor subtype may be responsible for inhibition of gastric emptying and motility. However, the site of action (central, peripheral, both) remains to be established.