We studied the acute effects of transmitter release induced by intracisternal (i.c.) 6-hydroxydopamine (6-OHDA) from mainly noradrenergic (NA) neurons and by 5,6-dihydroxytryptamine (5,6-DHT) from serotonergic (5HT) neurons. Each group of neurons affects blood pressure and heart rate in conscious rabbits through both suprapontine and bulbospinal pathways that alter both sympathetic and vagal function. Some of the pathways are complex with 5HT neurons and NA neurons in series with one another, while in others a given autonomic function is altered through parallel independent mechanisms. The central effects of α-methyldopa and clonidine on blood pressure and heart rate are mediated through both groups of neurons. We examined the role of the main bulbar NA neuron groups by producing bilateral electrolytic lesions of the A1, A2, A1 + A2, A5, and A6 + A7 regions, allowing time for degeneration and noting which component of the 6-OHDA transmitter release response had become affected by the lesion. These studies suggest that each is an integrative site with distinctive NA projections to the different autonomic motoneuron pools. We also examined how physiological changes in plasma levels of angiotensin II (AII) modulate the properties of the baroreceptor-heart rate reflex. The vagal component of the reflex is depressed and this is mediated through the action of AII on peripheral vagal ganglia, so that less acetyl choline is released per nerve impulse. This provides one model of the mechanisms by which central peptide transmitters may alter the action of other transmitters.
Address correspondence and reprint requests to Dr. P. I. Korner, at Baker Medical Research Institute, Commercial Road, Prahran, Victoria 3181, Australia.
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