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 system of the brain with important connections with other nuclei involved in cardiovascular function. Clonidine has been reported to produce its cardiovascular effects through an interaction with opioid and alpha 2-adrenergic receptors. The present study examined the arcuate nucleus as a site of action of clonidine. Male spontaneously hypertensive rats were anesthetized with pentobarbital and were instrumented for the measurement of blood pressure and heart rate. Cannulae were placed either through the cisterna magna (IC) or in the arcuate nucleus. Administration of clonidine (0.03-3.75 micrograms, IC) produced a dose-dependent hypotension and bradycardia. Pretreatment with naloxone (30 micrograms, IC) prior 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 to the central administration of clonidine did not alter the cardiovascular effects of clonidine. These results support the role of central opioidergic receptors in the cardiovascular effects of clonidine but do not support the arcuate nucleus as the site of action.