Cardiovascular functions of brain serotonergic neurons in the rabbit as analysed from the acute and chronic effects of 5,6-dihydroxytryptamine.

The effects of intracisternal (i.c.) 5,6-dihydroxytryptamine (5,6-DHT) or creatinine sulphate vehicle on mean arterial pressure (MAP), heart rate, and baroreceptor-heart rate and nasopharyngeal reflex properties were studied in conscious rabbits. For the baroreflex we derived sigmoid MAP-heart period (HP) curves, and for the nasopharyngeal reflex we measured apnea time, rise in HP, and delta MAP. The acute effects occurring over the first few hours in intact and decerebrate rabbits included: (a) tachycardia and a decrease in baroreflex HP range and gain, which were mediated through bulbar or spinal pathways influencing vagal motoneurons; (b) a transient early rise in MAP through a bulbar or spinal pathway and a late suprapontine rise in MAP; and (c) shorter apnea time, less bradycardia, and less well-maintained MAP during nasopharyngeal stimulation. By day 14, when spinal cord serotonin was depleted by 70%, resting MAP and heart rate had recovered, HP range and gain had risen above initial control, but nasopharyngeal apnea time and bradycardia were still reduced. Some of the acute responses were due to synaptic release of serotonin (5HT); since the tachycardia and late component of the pressor response were blocked by pretreatment with i.c. methysergide, the acute changes in baroreflex parameters were opposite to the chronic changes, and a second injection of 5,6-DHT failed to produce these changes. On the other hand, the acute and chronic nasopharyngeal responses were similar, suggesting that the former were due to neuronal block and not 5HT release. These findings indicate that central serotonergic neurons inhibit cardiac vagal activity, increase blood pressure through both suprapontine and bulbar or spinal pathways, and are involved in the nasopharyngeal reflex.