Chronic lability of arterial pressure produced by destruction of A2 catecholaminergic neurons in rat brainstem.

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Abstract
The cardiovascular effects of electrolytic lesions of the A2 group of catecholaminergic neurons of the dorsal medulla were analyzed in chronically instrumented rats. A2 lesions resulted after 24 h, in an enduring increase in lability (variability) and augmented reactivity of the arterial pressure during spontaneous or elicited behaviors, without a change in the average arterial pressure. Heart rate and its variability were unchanged. A2 lesions almost abolished the bradycardia elicited by acutely elevating arterial pressure with phenylephrine, but not the hypotension elicited under anesthesia by carotid sinus stretch. Lability of arterial pressure could not be attributed to damage to cardiovagal neurons. Vagal blockade with atropine or methylatropine did not alter the mean or variability of the arterial pressure. Lability of arterial pressure was produced only by damage to A2 neurons and not by lesions in the area postrema or by transection of commissural fibers of the nucleus tractus solitarii. The magnitude of lability was correlated directly with the amount of damage to A2. A2 lesions resulted in a reduction of dopamine-.beta.-hydroxylase activity to 60% of control in the NTS. Destruction of A2 neurons apparently produces persistent lability and exaggerated reactivity of arterial pressure as a consequence of partial removal of the noradrenergic innervation of the NTS. Noradrenergic neurons of A2 may serve to modulate baroreceptor reflexes in NTS. That lability of arterial pressure can occur in the absence of changes of average arterial pressure suggests distinctive anatomical networks subserving phasic and tonic control of the arterial pressure in the brainstem.