The involvement of gigantocellular reticular nucleus in clonidine-promoted hypotension and bradycardia in experimentally-induced hypertensive cats

The possible involvement of the medullary gigantocellular reticular nucleus (GRN) in clonidine-induced hypotension and bradycardia was examined in eats that were anesthetized with chloralose-urethane and were rendered experimentally hypertensive by a sustained bilateral common carotid artery occlusion. Clonidine (10 μ/kg i.v.) elicited an initial, transient hypertension, followed by a significant and maintained decrease in arterial blood pressure, accompanied by a marked reduction in heart rate. The same injection produced only a significant transient vasopression without subsequent discernible hypotension and bradycardia in cats receiving a focal electrolytic lesion of the GRN. On the other hand, microinjection of clonidine directly into the GRN, at an ineffective systemic dose (0.5 μg/kg), produced significant and prolonged vasodepression and cardioinhibition without the initial hypertension. Furthermore, the suppressive effects of clonidine, administered intravenously or directly into the GRN, on arterial blood pressure and heart rate, were substantially antagonized by bilateral cervical vagotomy or atropine sulfate (1 mg/kg i.v.). It is concluded that the GRN may be a strong candidate as the mediator of both clonidine-elicited hypotension and bradycardia, possibly using the vagal mechanism as its link to the cardiovascular effectors.