TY - T1的血管紧张素转换酶2和血管紧张素(1 - 7)轴在肺动脉高血压JF -欧洲呼吸杂志》乔和J - 10.1183/13993003.02416 -2019欧元六世- 56 - 1 SP - 1902416 AU胡里奥·桑多瓦尔盟-莱昂纳多Del Valle-Mondragon盟-费利佩•美索盟Nayeli Zayas AU -托马斯Pulido盟里卡多Teijeiro AU -赫Gonzalez-Pacheco盟然而Olmedo-Ocampo AU -卡洛斯Sisniega盟婀瑞思利Paez-Arenas盟Gustavo Pastelin-Hernandez AU -穆Gomez-Arroyo盟诺伯特·f·Voelkel Y1 - 2020/07/01 UR - //www.qdcxjkg.com/content/56/1/1902416.abstract N2 -背景在肺动脉高血压动物模型(PAH),血管紧张素转换酶(ACE) 2和血管紧张素(Ang) -(1 - 7)已被证明有常,抗增殖、antifibrotic antihypertrophic属性。然而,ACE2-Ang的地位和作用在人类PAH(1 - 7)轴是不完全理解。方法:我们对85名患者的诊断多环芳烃的截然不同的目的。55健康献血者的年龄和性别配对担任控制。血样经肺动脉在PAH患者右心catheterisation。对两组外周血得到。和(1 - 7)和——毛细管电泳测定使用区域。醛固酮,和(1 - 9),AngA和ACE2使用ELISA测定,决心保持酶和ACE2活动。47岁的85名患者的结果特发性PAH, 25多环芳烃与先天性心脏病相关,13多环芳烃与胶原血管疾病有关。控制相比,患者多环芳烃浓度较高AngII(平均1.03,四分位范围0.72 - -1.88 pmol·毫升−1和0.19,0.10 - -0.37 pmol·毫升−1;术;醛固酮0.001)和(88.7,58.7 -132 ng·dL−1和12.9,9.55 - -19.9 ng·dL−1; p<0.001). Conversely, PAH patients had a lower concentration of Ang(1–7) than controls (0.69, 0.474–0.91 pmol·mL−1 versus 4.07, 2.82–6.73 pmol·mL−1; p<0.001), and a lower concentration of Ang(1–9) and AngA. Similarly, the ACE2 concentration was higher than in controls (8.7, 5.35–13.2 ng·mL−1 versus 4.53, 1.47–14.3 ng·mL−1; p=0.011), whereas the ACE2 activity was significantly reduced (1.88, 1.08–2.81 nmol·mL−1 versus 5.97, 3.1–17.8 nmol·mL−1; p<0.001). No significant differences were found among the three different aetiological forms of PAH.Conclusions The AngII–ACE2–Ang(1–7) 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 (1–7)-MAS axis. Analysis of blood samples also demonstrates the presence of antibodies directed against ACE2 https://bit.ly/3alEbnJ ER -