The actions of intravenous clonidine [2-(2,6 dichlorophenylamino)-2-imidazoline hydrochloride] on blood pressure and heart rate were examined in conscious rabbits. Complete transection of the cervical spinal cord increased the intensity and duration of the hypertensive effect of 30 μg/kg of clonidine and completely abolished the fall in blood pressure. Heart rate slowing by clonidine was reduced. Results were similar 1 hour, 24 hours and 7 days after cord transection. Bilateral aortic and carotid sinus nerve section (baroreceptor deafferentation) increased both the hypertensive and hypotensive action of clonidine but reduced the bradycardia. When cervical cord transection was combined with baroreceptor deafferentation, the effect of clonidine on heart rate, and the hypotensive action, were abolished. It is concluded, that whereas the hypertensive action results from a direct effect on peripheral adrenoceptors, the fall in blood pressure is related to a reduction in sympathetic tone mediate mediated the level of the brain stem or more rostrally. The heart rate slowing results from both a reduction in sympathetic tone and also an enhanced vagal outflow. The increase in vagal tone seems to be dependent on the integrity of baroreceptor afferent pathways.
|Number of pages||7|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|Publication status||Published - 1 Jul 1977|