Korner P I, Badoer E, Head G A
Baker Medical Research Institute, Melbourne, Australia.
Brain Res. 1987 Dec 1;435(1-2):258-72. doi: 10.1016/0006-8993(87)91609-x.
We examined the role of the noradrenergic (NA) neurons of the A1, A2, A1 + A2, A5 and A6 + A7 regions on mean arterial pressure (MAP) and heart rate (HR), by comparing the acute responses of chronically lesioned and sham-operated rabbits to intracisternal 6-hydroxydopamine (6-OHDA, 600 micrograms/kg) which induces central release of transmitter. We studied rabbits (1) with intact arterial baroreceptors (non-denervated) and (2) after sino-aortic denervation (SAD). The acute transmitter release response consisted of an early fall in MAP (observed in SAD rabbits) and a late rise in MAP (observed in both non-denervated and SAD rabbits). Medullary lesions had no effect on either MAP component, but A5 and A6 + A7 lesions attenuated both pressor and depressor responses. Normally the transmitter release-induced MAP responses are modified by baroreceptor feedback. The 6-OHDA-induced HR changes were vagal in non-denervated rabbits and were sympathetically mediated in SAD rabbits. In non-denervated rabbits, A1, A2 and A1 + A2 lesions affected mainly the early vagal component, whilst A6 + A7 lesions affected the late vagal component. In SAD rabbits the early bradycardia was due to sympathetic inhibition and the late tachycardia due to sympathetic excitation; A1 + A2 lesions and A5 lesions attenuated the sympathetic bradycardia. We conclude that the various components of the MAP and HR responses are mediated through distinctive NA pathways; the deficits of a given lesion could be due to either to loss of NA cell bodies or of NA fibers of passage.
