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

Abstract

In the thyroid gland, vasoactive intestinal peptide (VIP) and acetylcholine (ACh) are found in nerve fibers associated with secretory cells and blood vessels. We have, therefore, initiated studies to explore the actions of and interactions between cholinergic agents and VIP in the regulation of thyroid vascular conductance (VC). Thyroid and other organ blood flows were measured using radiolabelled (¹⁴¹Ce) microspheres injected directly into the left cardiac ventricle of anesthetized male rats. The mean systemic arterial pressure was monitored and used in the calculation of organ VC (blood flow/arterial pressure). Plasma TSH, T3, and T4 levels before and after infusions were measured by RIA. The acute administration of ACh (3 × 10^-8 mol/l00 g BW) over 4 min increased thyroid VC, whereas nicotine (10^–7 mol/l00 g BW) had no such effect. Circulating TSH and thyroid-hormone levels following ACh or nicotine were not different from those in vehicle-treated animals at 20 min or 2 h after infusion. This observation suggested that ACh acts through muscarinic receptors at the thyroid gland to increase VC. In order to extend these observations and to evaluate whether VIP might exert any of its thyroidal effects on VC via muscarinic receptors, we assessed the effects of ACh, methacholine chloride (MCC), and VIP in the presence and absence of the muscarinic receptor blocker atropine. Rats were treated intravenously with saline or atropine (3 mg/kg) 20 min before intravenous infusions of vehicle, ACh (3 × 10^–8 mol/100 g BW), MCC (5 × 10^–9 mol/l00 g BW), or VIP (10 n mol/l00 g BW). Muscarinic blockade prevented the ACh-induced rise in thyroid VC, whereas the vasodilatory effect of VIP was greater if the rats were pretreated with atropine. These results are consistent with the hypothesis that VIP and ACh exert their effects at the thyroid gland through independent mechanisms. Furthermore, there appears to be an antagonistic interaction between cholinergic agents and VIP in the regulation of thyroid VC.

Thyroid receptor β involvement in the effects of acute nicotine on hippocampus-dependent memory

“…The effects of acute nicotine on thyroid function and thyroid hormone receptor (TR) signaling is largely unknown. Animal models suggest that acute nicotine administration did not directly alter thyroid hormone levels ( Cam and Bassett 1983 ; Huffman et al 1991 ), but did reduce TSH levels ( Andersson et al 1988 ), which is usually indicative of higher thyroid hormone levels. Further, levels of brain thyroid hormones may be independent of serum hormone concentrations, and brain TR activity may not correspond perfectly to serum hormone levels.…”