Cholinergic and VIPergic vasodilator actions of parasympathetic nerves on the thyroid blood flow in rats.

Abstract

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 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).

Muscarinic Modulation of the Vasodilatory Effects of Vasoactive Intestinal Peptide at the Rat Thyroid Gland

“…In our experiments, this blockade at muscarinic sites was panic-ularly effective, as indicated by the finding that all ACh-induced increases in organ VCs were abolished following atropine pre treatment. Our finding regarding the maintenance of thyroidal effects of VIP after muscarinic blockade, when coupled with the observation that thyroid VIP output can increase during the stimulation of parasympathetic nerves [9], makes VIP a prime candidate for the atropine-resistant vasodilation seen during parasympathetic-nerve stimulation in this gland [9].…”

“…Since the dose-response curve for VIP is very steep [12,13], such a combination of endogenous and exogenous VIP might well result in enhanced thyroid VC. While Ito et al [9] did not observe changes in thyroidal VIP secretion rates after atropine pretreatment in rats, any such effects appear to depend upon the on-going stimulation rate. Thus, in the cat salivary gland, this effect was observed during stimulations of 6 or 15 Hz, but not at 2 Hz [22].…”

“…The parasympathetic nervous system appears to play a role in the regulation of thyroidal vasomotor tone, since increases in thyroid BF have been described following vagal or superiorlaryngeal-nerve stimulation [5,9,17]. The participation of ACh and VIP in these parasympathetic responses is suggested by ob servations that both of these substances can increase thyroid BF [5,9,12,13], and that muscarinic blockade can partially, but not completely, abolish the increases in thyroid BF seen during parasympathetic-nerve stimulation [9].…”

“…The participation of ACh and VIP in these parasympathetic responses is suggested by ob servations that both of these substances can increase thyroid BF [5,9,12,13], and that muscarinic blockade can partially, but not completely, abolish the increases in thyroid BF seen during parasympathetic-nerve stimulation [9]. In the present study, we provide evidence that ACh and VIP can independently modu late thyroid VC and suggest that there may be an antagonistic interaction between endogenous ACh and VIP in the regulation of thyroid VC,…”

“…Va soactive intestinal peptide (VIP) is among the peptides found in thyroid nerves of parasympathetic origin which terminate on blood vessels and in close proximity to follicular cells [8]. This peptide has also been implicated in the atropine-resistant va sodilation seen during parasympathetic-nerve stimulation of the thyroid gland [9]. However, the extent to which VIP and cholinergic agents interact in the regulation of thyroid function has not been fully explored.…”