Muscarinic modulation of the vasodilatory effects of vasoactive intestinal peptide at the rat thyroid gland.
Muscarinic modulation of the vasodilatory effects of vasoactive intestinal peptide at the rat thyroid gland.
复制标题
大鼠甲状腺血管活性肠肽的血管舒张作用的毒蕈碱调节。
DOI：
10.1159/000125699
复制
发表时间：
1991
影响因子：
4.1
通讯作者：
Hedge,GA
中科院分区：
文献类型：
--
作者：
Huffman,LJ;Michalkiewicz,M;Connors,JM;Pietrzyk,Z;Hedge,GA
在甲状腺中，血管活性肠肽（VIP）和乙酰胆碱（ACh）存在于与分泌细胞和血管相关的神经纤维中。因此，我们开始研究胆碱能药物和VIP在调节甲状腺血管传导（VC）中的作用及其相互作用。用放射性标记（141Ce）微球直接注射到麻醉的雄性大鼠左心室，测量甲状腺和其他器官的血流。监测平均全身动脉压并用于计算器官VC（血流量/动脉压）。采用RIA法测定输注前后血浆TSH、T3、T4水平。急性给予乙酰胆碱（3 × 10-8mol/l00 g BW）超过4 min，甲状腺VC增加，而尼古丁（10-7mol /l00 g BW）无此作用。注射后20分钟或2小时，乙酰氨基酚或尼古丁后的循环TSH和甲状腺激素水平与灌药后的动物没有差异。这一观察表明乙酰胆碱通过甲状腺的毒蕈碱受体增加VC。为了扩展这些观察结果并评估VIP是否可能通过毒蕈碱受体对VC发挥其甲状腺作用，我们评估了乙酰胆碱、甲基胆碱氯（MCC）和VIP在存在和不存在毒蕈碱受体阻滞剂阿托品的情况下的作用。大鼠在静脉滴注药体、乙酰胆碱（3 × 10 - 8mol/100 g BW）、MCC （5 × 10 - 9mol/ 100 g BW）或VIP （10 n mol/100 g BW）前20 min静脉滴注生理盐水或阿托品（3 mg/kg）。毒蕈碱阻断可阻止乙酰胆碱诱导的甲状腺VC升高，而阿托品预处理后VIP的血管扩张作用更大。这些结果与VIP和ACh通过各自独立的机制在甲状腺发挥作用的假设相一致。此外，胆碱能药物和VIP在甲状腺VC的调节中似乎存在拮抗相互作用。
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 × 10-8mol/l00 g BW) over 4 min increased thyroid VC, whereas nicotine (10–7mol/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 × 10–8mol/100 g BW), MCC (5 × 10–9mol/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.