Cardiovascular role of A1 catecholaminergic neurons in the rabbit. Effect of chronic lesions on responses to methyldopa, clonidine and 6-OHDA induced transmitter release.

We confirmed the findings of previous investigators that bilateral anodal lesions of the A1 region were associated with hypertension, bradycardia, pulmonary edema and a high mortality. All these sequelae (except the bradycardia) no longer occurred after cathodal lesions and these were therefore used to investigate the role of the catecholaminergic (CA) neurons of the A1 region in circulatory regulation. Conscious rabbits were studied 2-4 weeks after A1 lesions or sham-operation, when resting mean arterial pressure (MAP) and heart rate (HR) were closely similar in both groups. We tested for differences in MAP and HR responses between lesioned and sham-operated groups: to intracisternal (i.c.) alpha-methyldopa (MD) and to clonidine; and to the acute effects of i.c. 6-hydroxydopamine (6-OHDA) which elicits central CA release. Since these tests depend on the integrity of the central CA neurons, response differences between lesioned and sham-operated groups denote participation by the CA neurons of the A1 region in the central circulatory pathways. The bradycardia responses in the above tests were all smaller in lesioned than sham-operated rabbits, but there were no differences in MAP responses. Electrical stimulation of the region under alfathesin anaesthesia produced depressor responses at low frequencies and pressor responses at high frequencies. From the results in conscious rabbits CA neurons of the A1 region mainly influence the pathways regulating HR, rather than blood pressure. The changes in MAP during electrical stimulation are thus probably mediated through non-CA neurons.