Are opioid receptors involved in the bradycardiac and hypotensive action of clonidine?

Experimental evidence that supports or rejects an involvement of opioid receptors in the cardiovascular effects of clonidine was sought. In anesthetized rabbits, clonidine decreased blood pressure and heart rate. These effects were related to the clonidine dose. High doses of clonidine produced a biphasic response in blood pressure without resulting in a significant baroreflex. However, it was not difficult to produce hypotensive action of clonidine without the biphasic action using low doses of clonidine. A pretreatment of the animals with naloxone (1 mg/1 kg) prevented the hypotensive action of clonidine at low dose. This antagonistic action of naloxone against clonidine was also evident in other cardiac parameters such as heart rate and efferent sympathetic renal nerve activity. The antagonistic action was not demonstrably significant with the high doses of clonidine. The present study in normotensive anesthetized rabbits suggests that specific central interactions between opioid and adrenergic receptors can be demonstrated under defined conditions, although such interactions were reported in pathophysiologic conditions such as essential hypertension.