The action of clonidine on the baroreflex control of heart rate in conscious animals and man, and on single aortic baroreceptor discharge in the rabbit

Changes in mean arterial pressure (MAP) were produced in conscious rabbits by inflation of balloon cuffs previously implanted round the inferior vena cava and aorta Sigmoid stimulus/response curves (MAP/Heart Period, HP) were constructed. Clonidine caused a striking dose dependent increase in gain of the reflex arc in both normal rabbits and rabbits with renal hypertension. The largest effect was on vagal motorneurons but a similar but smaller effect was present in vagotomized animals. Similar changes in the baroreflex arc were produced by injection of very much smaller doses of clonidine into the lateral cerebral ventricle. Recordings made from single aortic baroreceptor fibers in anesthetized rabbits showed again a dose dependent sensitization. These results suggest that the bradycardia caused by clonidine is largely mediated via an action in the brain on the baroreflex arc, with an additional action on the baroreceptors themselves. Preliminary results in normal man showed a similar increase in the gain of this reflex after i.v. clonidine (150 μg).