OPIOIDERGIC RECEPTORS IN THE ARCUATE NUCLEUS ARE NOT INVOLVED IN THE CARDIOVASCULAR EFFECTS OF CLONIDINE

The arcuate nucleus is the bed nucleus for the pro-opiomelancortin sys tem of the brain with important connections with other nuclei involved in cardiovascular function. Clonidine has been reported to produce it s cardiovascular effects through an interaction with opioid and alpha( 2)-adrenergic receptors. The present study examined the arcuate nucleu s as a site of action of clonidine. Male spontaneously hypertensive ra ts were anesthetized with pentobarbital and were instrumented for the measurement of blood pressure and heart rate. Cannulae were placed eit her through the cisterna magna (IC) or in the arcuate nucleus. Adminis tration of clonidine (0.03-3.75 mu g, IC) produced a dose-dependent hy potension and bradycardia. Pretreatment with naloxone (30 mu g, IC) pr ior to clonidine administration resulted in a significant attenuation of both the clonidine-induced hypotension and bradycardia. In contrast , administration of naloxone (100 ng) into the arcuate nucleus prior t o the central administration of clonidine did not alter the cardiovasc ular effects of clonidine. These results support the role of central o pioidergic receptors in the cardiovascular effects of clonidine but do not support the arcuate nucleus as the site of action.