Functional and autoradiographic studies to locate the sites at which clonidine acts to cause hyperglycaemia and inhibition of opiate-induced sympathetic outflow.

Abstract

The effect of intracisternal administration of clonidine (1 microgram/kg) on the response to intravenous injection of morphine (4 mg/kg) was examined in conscious rabbits. Morphine acts on central opiate receptors to increase sympathetic outflow and cause hypertension. Clonidine, given intracisternally, prevented the morphine-induced rise in mean arterial pressure, fall in heart rate and increase in catecholamines in plasma. Using in vitro autoradiography, alpha 2-adrenoceptors were localised in the nucleus of the tractus solitarius and the dorsal motor nucleus of the vagus and these may be two of the sites at which clonidine acts. Clonidine also causes hyperglycaemia after intravenous admin..