The present experiment was performed to investigate the effect of stimulating the parasympathetic superior laryngeal nerve (SLN) on thyroid blood flow and its mediator substances in urethane-chloralose anesthetized rats. Thyroid blood flow was measured by counting number of blood drops from a thin catheter inserted into the thyroid vein. SLNs were cut bilaterally and their peripheral portions were electrically stimulated. Electrical stimulations (intensity, 10 V; pulse duration, 0.5 ms) of SLNs

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... increased thyroid blood flow in a frequency-dependent manner as stimulus frequencies increased from 2 to 40 Hz. The intravenous administration of atropine (0.5 mg/kg) reduced these responses, but did not abolish them. The basal secretion rate of vasoactive intestinal peptide (VIP). from thyroid glands in the resting state was nearly zero (0.25 ± 0.14 pg/(kg • min)). SLN stimulation increased markedly the VIP secretion rate to 3.40 + 0.64 pg/(kg • min). The VIP secretion responses evoked by SLN stimulation remained in atropinized rats. Furthermore, exogenously applied VIP increased the thyroid blood flow dosedependently. These results suggest that SLN stimulation increases the thyroid blood flow by dilating thyroid blood vessels via activation of cholinergic and non-cholinergic (probably VIP-containing) nerve fibers. Thus, these parasympathetic vasodilation systems may play a supplementary role in regulating the secretion of thyroid hormone by changing the thyroid blood flow in addition to the role of hormonal regulation by the thyroid stimulating hormone (TSH).