Actions by Angiotensin II on esophageal contractility in humans
Actions by Angiotensin II on esophageal contractility in humans
复制标题
DOI：
10.1053/j.gastro.2006.11.010
复制
发表时间：
2007-01-01
期刊：
影响因子：
29.4
通讯作者：
Fandriks, Lars
中科院分区：
文献类型：
--
作者：
Casselbrant, Anna;Edebo, Anders;Fandriks, Lars
背景和目标：血管紧张素11是一种有效的平滑肌激活剂，但对胃肠运动活性的研究还不多。本研究探讨了人食管肌肉组织中肾素-血管紧张素系统（RAS）的表达及血管紧张素II的作用。研究方法：食管体和下食管括约肌的肌肉标本来自因粘膜肿瘤而接受切除术的患者。健康志愿者参加了高分辨率测压和多次经粘膜评估食管动力的功能检查。电位差测量。结果：在食管肌肉组织中发现RAS关键组分的基因转录本。免疫组织化学显示，血管紧张素II 1型（AT（1））受体在肌肉束和血管壁中有明显的染色，而血管紧张素II 2型受体仅限于血管。血管紧张素II在体外引起浓度依赖性收缩，其可被AT 1受体拮抗剂氯沙坦抑制，但不被血管紧张素11 2型受体拮抗剂PD 123319抑制。AT受体拮抗剂坎地沙坦给药可降低吞咽诱导的蠕动收缩幅度以及食管胃交界处基线高压区的长度和压力幅度。坎地沙坦预处理既不影响吞咽诱导的轴向运动，也不影响短暂的下食管括约肌松弛后的收缩。结论：该研究证实了远端食管肌肉组织中的局部RAS，并且血管紧张素II是通过AT 1受体的食管收缩的有效刺激物。提示血管紧张素Ⅱ参与了人食管的生理调控。运动活动
Background & Aims: Angiotensin 11 is a potent activator of smooth muscles but has not been much investigated with regard to gastrointestinal motor activity. This study explores expression of the reninangiotensin system (RAS) in human esophageal musculature and actions by Angiotensin II both in vitro and in vivo. Methods: Muscular specimens of esophageal body and lower esophageal sphincter were obtained from patients undergoing resection as a result of mucosal neoplasm. Healthy volunteers participated in functional examinations of esophageal motility assessed by high-resolution manometry and multiple transmucosal. potential-difference measurements. Results: Gene transcripts of key components of RAS were found in the esophageal musculature. Immunohistochemistry revealed a distinct staining for Angiotensin II type 1 (AT(1)) receptors in the muscular bundles and blood-vessel walls, whereas Angiotensin II type 2 receptors were confined to blood vessels only. Angiotensin II caused concentration-dependent contractions in vitro, which were inhibited by the AT, receptor antagonist losartan but not by the Angiotensin 11 type 2 receptor antagonist PD123319. Administration of the AT, receptor antagonist candesartan reduced the amplitude of swallow-induced peristaltic contractions and both the length and pressure amplitude of baseline high-pressure zone at the esophagogastric junction. Neither swallow-induced axial movements, nor the contraction after transient lower esophageal sphincter relaxations, were influenced by candesartan pretreatment. Conclusions: The study demonstrates a local RAS in the musculature of the distal esophagus and that Angiotensin II is a potent stimulator of esophageal contractions via the AT, receptor. The results suggest that Angiotensin II participates in the physiological control of the human esophageal. motor activity.