Pharmacological investigation on the neurohumoral transmission of the vasomotor regulation.

Renal efferent sympathetic activity and its changes due to stimulation of the central stump of the vagal, sciatic and ulnar nerves were investigated. In addition, the effect on basal activity and sympathetic reflexes of drugs with well defined site of action was studied (diazepam, tofizopam, phentolamine, dihydroergotamine, chlorpromazine, reserpine, clonidine, atropine, methysergide and phenindamine). The sympathetic efferent activity and the changes in sympathetic reflexes allowed conclusions to be drawn as to the functional state of the vasomotor centre. Neither methysergide nor phenindamine inhibited efferent sympathetic activity or influenced sympathetic reflexes. These findings exclude the possibility of serotonin or histamine being the transmitter substance in the vasomotor neurone. Experiments with atropine revealed that the muscarinic action of acetylcholine does not figure in the sympathetic inhibitory or excitatory reflex processes. Of the drugs investigated only diazepam and clonidine inhibited efferent sympathetic activity. Clonidine was more selective and acted in much lower doses (20 micrograms/kg) than diazepam (0.5--1 mg/kg). The alpha blocking agents inhibited the viscero-sympathetic inhibitory reflex arch more intensely than the somato-sympathetic inhibitory one. The transmitter is presumably noradrenaline. The sympathetic excitatory reflexes were decreased by diazepam and tofizopam and increased by clonidine and phentolamine. The other substances were ineffective. As to the transmitter substance figuring in the sympathetic excitatory reflexes no unequivocal answer could be obtained in the present experiments.