Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats
Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats
复制标题
神经肽 Y 通过大鼠左背迷走神经复合体中的 Y1 受体刺激胆汁分泌
作者：
M. Yoneda;K. Nakamura;S. Yokohama;K. Tamori;Yoichi Sato;K. Aso;M. Aoshima;Toru Kono;I. Makino
在动物模型中，将神经肽 Y (NPY) 注射到脑脊液和左背迷走神经复合体中，可通过迷走神经毒蕈碱途径增强不依赖胆汁酸和依赖碳酸氢盐的胆汁分泌。 NPY 结合并激活六种不同的受体亚型，NPY Y1 和 Y2 受体分布在背侧迷走神经复合体中。我们试图通过检查将特定 NPY 受体激动剂显微注射到背侧迷走神经复合体中的效果来确定哪些 NPY 受体亚型参与胆汁分泌的中枢刺激。对氨基甲酸乙酯麻醉且胆汁酸补偿的大鼠进行胆管插管。测量基础分泌后，将 NPY、肽 YY (PYY)、[Leu31、Pro34]NPY、NPY(13-36) 或 NPY(3-36) 显微注射到右侧或左侧背迷走神经复合体中，观察胆汁分泌 100 分钟。在肽注射前2小时进行肝分支迷走神经切断术。将 NPY 和 PYY (8 pmol) 显微注射到左背迷走神经复合体中会增加胆汁分泌。 [Leu31, Pro34]NPY 显微注射到左背迷走神经复合体中，也会剂量依赖性 (1-8 pmol) 刺激不依赖胆汁酸和依赖碳酸氢盐的胆汁分泌。将 NPY(13-36) 显微注射到左背迷走神经复合体中不会刺激胆汁分泌，并且 NPY(3-36) 会剂量依赖性地抑制胆汁分泌。 [Leu31, Pro34]NPY 对胆汁分泌的刺激被肝分支迷走神经切断术消除。 NPY 在左背迷走神经复合体中发挥作用，通过 Y1 受体亚型刺激不依赖胆汁酸和依赖碳酸氢盐的胆汁分泌。
Neuropeptide Y (NPY) injected into the cerebrospinal fluid and the left dorsal vagal complex enhances bile acid–independent and bicarbonate‐dependent bile secretion through vagal muscarinic pathways in animal models. NPY binds to and activates six different receptor subtypes, and NPY Y1 and Y2 receptors are distributed in the dorsal vagal complex. We sought to determine which NPY receptor subtypes are involved in central stimulation of bile secretion by examining the effect of microinjection of specific NPY receptor agonists into the dorsal vagal complex. The bile duct was cannulated in urethane‐anesthetized and bile acid–compensated rats. After measuring basal secretion, NPY, peptide YY (PYY), [Leu31, Pro34]NPY, NPY(13‐36), or NPY(3‐36) was microinjected into the either right or left dorsal vagal complex and bile secretion was observed for 100 minutes. Hepatic branch vagotomy was performed 2 hours before the peptide injection. Microinjection of NPY and PYY (8 pmol) into the left dorsal vagal complex increased bile secretion. [Leu31, Pro34]NPY microinjected into the left dorsal vagal complex also dose‐dependently (1‐8 pmol) stimulated bile acid–independent and bicarbonate‐dependent bile secretion. Microinjection of NPY(13‐36) into the left dorsal vagal complex did not stimulate and NPY(3‐36) dose‐dependently inhibited bile secretion. Stimulation of bile secretion by [Leu31, Pro34]NPY was abolished by hepatic branch vagotomy. NPY acts in the left dorsal vagal complex to stimulate bile acid–independent and bicarbonate‐dependent bile secretion via Y1 receptor subtype.
DOI：
10.1152/ajpgi.1995.268.1.g1
发表时间：
1995
期刊：
The American journal of physiology
影响因子：
--
作者：
R. Rogers;D. McTigue;G. Hermann
通讯作者：
R. Rogers;D. McTigue;G. Hermann
脑干核中的 PYY 诱导大鼠迷走神经刺激胃酸分泌。
DOI：
10.1152/ajpgi.1995.268.6.g943
发表时间：
1995
期刊：
The American journal of physiology.
影响因子：
--
作者：
Yang,H;Tache,Y
通讯作者：
Tache,Y
脑室内神经肽 Y 通过迷走神经机制刺激胆汁分泌。
影响因子：
24.5
作者：
Farouk,M;Geoghegan,JG;Pruthi,RS;Thomson,HJ;Pappas,TN;Meyers,WC
通讯作者：
Meyers,WC