Differences between mechanisms of noradrenaline and clonidine-induced emesis in cats

Abstract

Both noradrenaline and clonidine, injected into the cerebral ventricles, induced dose-dependent and shortlasting emesis in cats. Intracerebroventricular yohimbine, but not prazosin, inhibited the emesis evoked by noradrenaline. In contrast, both intracerebroventricular yohimbine and prazosin did not significantly change the clonidine-induced emesis. The ablation of the area postrema impaired the noradrenaline, but not the clonidine-induced emesis. It is postulated that the emesis produced by noradrenaline is mediated through alpha-2 adrenoceptors within the area postrema, whereas clonidine acted on emetic detectors outside chemoreceptor trigger zone in the area postrema most probably within the brainstem areas. These detectors are at least as sensitive to emetic stimuli as those within the area postrema. Moreover, chemical stimuli originating from the cerebrospinal fluid can induce emesis through these detectors without the area postrema.