Participation of Central Noradrenergic Neurons in Arterial Baroreceptor Reflexes in the Rabbit: A STUDY WITH INTRACISTERNALLY ADMINISTERED 6-HYDROXYDOPAMINE

Rabbits were given intracisternal injections of 6-hydroxydopamine (6-OH-DA) that caused selective ablation of central noradrenergic neurons without damaging peripheral sympathetic nerves. Administration of 6-OH-DA (600 µg/kg, intracisternally) to normal rabbits produced a permanent bradycardia of about 30%, which was initiated centrally and mediated mainly through the vagus, and caused a brief reduction in mean arterial blood pressure, which was due to transient withdrawal of alpha-sympathetic tone. Treatment with 6-OH-DA (600 µg/kg) completely prevented the increases in arterial blood pressure seen on the seventh and the fourteenth day after sinoaortic denervation in control rabbits, although there was a transient increase in blood pressure for 1 day after denervation in the group treated with 6-OH-DA. Central norepinephrine concentrations were reduced in all areas, especially in the spinal cord (to less than 10% of control), in the denervated rabbits treated with 6-OH-DA compared with the levels in denervated controls. When 6-OH-DA (600 µg/kg, intracisternally) was given to rabbits with neurogenic hypertension produced by buffer nerve section, it caused an immediate and persistent return of pressure to the level that existed before denervation. Probably, the integrity of central noradrenergic neurons is necessary for the development of sustained increases in arterial blood pressure following sinoaortic denervation. We suggest that central noradrenergic nerves form an essential link in the baroreceptor reflex arc, possibly at the bulbospinal level.