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Two models of peripheral sympathetic autoregulation: role of neuronal histamine.

We have studied the influence of a peripheral histamine-containing neuronal system on the sympathetic activity of the rat vas deferens. Chronic surgical interruptions of the sympathetic structures involving the adjacent histamine-containing neuronal system cause changes of sympathetic activity, as measured by the rate of disappearance of norepinephrine after reserpine administration to the awake rat. Sympathetic ganglionectomy performed on either side causes an enhancement of the sympathetic activity in the contralateral vas deferens. When the decussation of histamine-containing pathways is surgically interrupted (interganglionic section), a bilateral enhancement of sympathetic activity occurs. The histamine-containing neuronal system seems to exert a contralateral reciprocal inhibitory modulation of sympathetic activity at the vas deferens. This modulation is evoked by nervous impulses traveling in the preganglionic fiber because enhancement of sympathetic activity due to contralateral ganglionectomy is suppressed by ipsilateral decentralization. No compensatory reflexes of central origin are observed. Sympathetic enhancement due to interruption of histamine-containing nervous pathways is reversed by i.v. infusion of histamine. An H-1 or H-2 histamine receptor antagonist does not have any effect on the vas deferens sympathetic activity of the intact rat. In the heart of the deafferentated dog, removal of the left stellate sympathetic ganglion causes facilitation of the chronotropic responses induced by stimulation of the right sympathetic postganglionic nerve, also suggesting a peripheral contralateral inhibitory modulation of sympathetic activity at the heart. It appears from all these findings that a peripheral inhibitory reflex is evoked when sympathetic activity is enhanced, thus contributing to maintaining homeostasis.