Central α2-adrenergic control of the pattern of small intestinal motility in rats

Abstract

The effects of central and peripheral administration of α2-adrenoceptor agonists and antagonists on small intestinal motility were examined in conscious rats chronically fitted with electrodes implanted in the duodenojejunal wall and a cannula placed in a cerebral lateral ventricle. In fasted rats, intracerebroventricular or intraperitoneal administration of clonidine (5 μg) immediately disrupted the migrating myoelectric complex pattern with a total inhibition of spiking activity during the first hour, followed by a period of irregular spiking activity for 2 h. The inhibition was abolished by previous intramuscular administration of yohimbine (600 μg), and the period of irregular activity was suppressed by intracerebroventricular yohimbine (30 μg). Naphazoline, an α2-agonist that poorly crosses the blood-brain barrier, only inhibited spiking activity when administered intraperitoneally (1 μg) and induced only a period of irregular spiking activity when administered intracerebroventricularly at the same dose. In fed rats, intracerebroventricular administration of yohimbine or phentolamine (30 μg), and to a lesser extent prazosin, restores a migrating myoelectric complex pattern typical of the fasted state. Peripheral administration of these three antagonists at a dose 20 times higher was ineffective. Finally, both feeding and central administration of α2-agonists disrupt the migrating myoelectric complex pattern. Such pharmacologic data suggest a possible role of central α2-adrenoceptors in the regulation of intestinal motility in rats.