The effects of clonidine (Catapres®) on the baroreceptor-heart rate reflex were studied in unanaesthetized rabbits, and its action on single aortic baroreceptor fibre discharge was examined under anaesthesia. Intravenous clonidine (bolus 2.5 to 10 μg/kg + infusion of 0.25 to 1.5 μg/kg/min) altered the mean arterial pressure (MAP) - heart period (HP; pulse interval) curve, reducing median blood pressure and increasing the gain and heart period range (HPR). At low dose increased HPR by enhancing both vagal excitation and sympathetic inhibition of HP during a rise in MAP, compared with control conditions. At high i.v. dose of drug sympathetic inhibition was complete even at low MAP, and HPR increased due to a rise in vagal output to 4-6 times control. Lateral ventricle injections of 0.5 to 1.5 μg/kg of clonidine altered MAP - HP curve parameters in a similar manner as i.v. infusion. High dose of clonidine i.v. enhanced single aortic baroreceptor fibre discharge at a given MAP in anaesthetized animals, but there was no effect at low dose. Clonidine alters heart rate mainly through its direct central action on the baroreceptor pathways; at high dose these effects are reinforced by peripheral baroreceptor resetting. Clonidine has only slight effects on cardiac motoneurones not receiving baroreceptor projections.
- Baroreflex dependent effect
- Baroreflex independent effect
- Cardiac sympathetic efferents
- Central baroreflex resetting
- Peripheral baroreflex resetting
- Vagal efferents