The influence of the trigeminal ganglion on carotid blood flow in anaesthetized guinea-pigs.

1. The influence of the trigeminal ganglion on the carotid circulation has been investigated by measuring electrical stimulation-induced alterations in carotid arterial blood flow and resistance in anaesthetized guinea-pigs. The effects of several receptor antagonists were assessed to determine which neurotransmitters are involved in regulating carotid blood flow. 2. Arterial blood pressure and carotid vascular resistance were reduced by electrical stimulation (0.5 mA, 1 ms, 5 Hz, 60 s) of the trigeminal ganglion ipsilateral to the carotid artery from which flow was measured. No consistent effect of electrical stimulation on carotid blood flow was observed. However, when guinea-pigs were pretreated with guanethidine (30 mg kg-1, s.c., 24 h prior to experiments), stimulation produced little change in blood pressure, while carotid blood flow was increased and vascular resistance decreased, consistent with vasodilatation in the cranial circulation. Stimulation of the trigeminal ganglion contralateral to the carotid artery from which blood flow was measured, had little effect on either carotid blood flow or vascular resistance. 3. In animals pretreated with guanethidine, intravenous administration of the vasoactive intestinal polypeptide (VIP) receptor antagonist, [p-Cl-D-Phe6,Leu17]-VIP (50 micrograms kg-1) significantly attenuated the increase in carotid blood flow and decrease in carotid vascular resistance evoked by trigeminal ganglion stimulation. Responses evoked by trigeminal ganglion stimulation were, however, unaffected by intravenous injection of the tachykinin NK1 receptor antagonists, GR82334 (0.3 mg kg-1) and CP-99,994 (0.4 mg kg-1), calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP8-37 (0.9 mg kg-1) and the ganglion blocking agent, hexamethonium (10 mg kg-1). 4. It is concluded that in the guanethidine-pretreated guinea-pig, electrical stimulation of the trigeminal ganglion increases carotid blood flow and produces an accompanying decrease in carotid vascular resistance, consistent with the dilatation of carotid blood vessels. The transmitter mediating this effect is most likely to be VIP.