Action of the morphinometic agent, fentanyl, on the nucleas tractus solitarii and the nucleus ambiguus cardiovascular neurons.

Using extracellular recordings, the discharges of blood pressure dependent neurons were detected in the nucleus tractus solitarii (NTS) and in the nucleus ambiguus (NA) of anesthetized dogs. Type A blood pressure dependent neurons (sympathoinhibitory or vagoexcitatory neurons) were detected when their firing rates were increased during i.v. noradrenaline and when their firing rates were reduced or abolished during bilateral carotid occlusion. Type B blood pressure dependent neurons (sympathoexcitatory neurons or vagoinhibitory neurons) were identified when their firing rates were reduced or when firing was abolished during the rise in blood pressure induced by noradrenaline and when their firing rates were increased during bilateral carotid occlusion. Baroreceptor neurons were identified when neuronal activity with cardiac rhythm, was detected in the NTS. Fentanyl (20 micrograms/kg i.v.) decreased the spontaneous firing rate of type A neurons found in the NTS. In contrast, fentanyl altered in two opposite ways the firing rate of neurons classified as type A and found in the NA. In the first group of type A neurons, fentanyl induced a marked increase in firing rates. A second group of type A neurons in the NA responded to fentanyl by a reduction in firing rates. Fentanyl reduced the firing rate of type B neurons detected in the NTS and the NA. Fentanyl (20 micrograms/kg i.v.) induced biphasic changes in the firing rate of baroreceptor neurons detected in the NTS. The effects of fentanyl on blood pressure, heart rate and firing rate of all types of cardiovascular neurons were antagonized by naloxone.