@Article {Sandoval1902416，作者= {Sandoval，Julio和Del Valle-Mondrag {\'o} N，Leonardo和Masso，Felipe和Zayas，nayeli和nayeli和pulido，tom {\'a} an} and teijeiro and teijeiro and teijeiro and teijeiros and ricardo and ricardo and ricadoz pacheco，Hector和Olmedo-Ocampo，Rossana和Sisniega，Carlos和Paez-Arenas，Araceli，Araceli和astelin-Hernandez，Gustavo和Gomez-Arroyo，Jose and Jose and Jose and Voelkel，Norbert F.}\ textendash} 7）肺动脉高压}中的轴，音量= {56}，number = {1}，Elocation-id = {1902416}，年= {2020}，doi = {10.1183/13993003.02416-2019}{188bet官网地址欧洲呼吸社会}，摘要= {肺动脉高压动物模型（PAH），血管紧张素转换酶（ACE）2和血管紧张素（ANG） - （1 {\ textendendash} 7）抗增生性，抗纤维化和抗肿瘤特性。但是，人类PAH中ACE2-ang（1 {\ textEndEndash} 7）轴的状态和作用是不完全理解的。我们研究了85例患者，并诊断出具有不同病因的PAH。55个健康的血液捐献者成熟，性别为对照。在右心导管插入期间，PAH患者的肺动脉中获得了血液样本。两组均获得外周血。使用区域毛细管电泳测量ANG（1 {\ textendash} 7）和-II。使用ELISA测量醛固酮，ANG（1 {\ Textendash} 9），ANGA和ACE2，并通过酶酶确定ACE2活性。在85例患者中，有47例患有特发性PAH，25例患有PAH与先天性心脏病相关，13例患有PAH。 associated with collagen vascular disease. Compared to controls, patients with PAH had a higher concentration of AngII (median 1.03, interquartile range 0.72{\textendash}1.88 pmol{\textperiodcentered}mL-1 versus 0.19, 0.10{\textendash}0.37 pmol{\textperiodcentered}mL-1; p\<0.001) and of aldosterone (88.7, 58.7{\textendash}132 ng{\textperiodcentered}dL-1 versus 12.9, 9.55{\textendash}19.9 ng{\textperiodcentered}dL-1; p\<0.001). Conversely, PAH patients had a lower concentration of Ang(1{\textendash}7) than controls (0.69, 0.474{\textendash}0.91 pmol{\textperiodcentered}mL-1 versus 4.07, 2.82{\textendash}6.73 pmol{\textperiodcentered}mL-1; p\<0.001), and a lower concentration of Ang(1{\textendash}9) and AngA. Similarly, the ACE2 concentration was higher than in controls (8.7, 5.35{\textendash}13.2 ng{\textperiodcentered}mL-1 versus 4.53, 1.47{\textendash}14.3 ng{\textperiodcentered}mL-1; p=0.011), whereas the ACE2 activity was significantly reduced (1.88, 1.08{\textendash}2.81 nmol{\textperiodcentered}mL-1 versus 5.97, 3.1{\textendash}17.8 nmol{\textperiodcentered}mL-1; p\<0.001). No significant differences were found among the three different aetiological forms of PAH.Conclusions The AngII{\textendash}ACE2{\textendash}Ang(1{\textendash}7) axis appears to be altered in human PAH and we propose that this imbalance, in favour of AngII, plays a role in the pathogenesis of the severe PAH. Further mechanistic studies are warranted.This study demonstrates that in patients with PAH of different aetiologies there are alterations of the ACE2-angiotensin (1{\textendash}7)-MAS axis. Analysis of blood samples also demonstrates the presence of antibodies directed against ACE2 https://bit.ly/3alEbnJ}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/56/1/1902416}, eprint = {//www.qdcxjkg.com/content/56/1/1902416.full.pdf}, journal = {European Respiratory Journal} }