内分泌学
内科学
血管紧张素Ⅱ受体1型
血管紧张素II
肾素-血管紧张素系统
受体
肺
缺氧(环境)
血管紧张素转换酶
血管紧张素转化酶2
肺动脉高压
转基因
化学
医学
血压
基因
生物化学
2019年冠状病毒病(COVID-19)
疾病
氧气
传染病(医学专业)
有机化学
作者
Václav Hampl,J Herget,J Bíbová,Alena Baňasová,Zuzana Husková,Zdeňka Vaňourková,Šárka Jíchová,Petr Kujal,Zdeňka Vernerová,Janusz Sadowski,Luděk Červenka
出处
期刊:Physiological Research
[Institute of Physiology of the Czech Academy of Sciences]
日期:2015-02-15
卷期号:: 25-38
被引量:53
标识
DOI:10.33549/physiolres.932861
摘要
The present study was performed to evaluate the role of intrapulmonary activity of the two axes of the renin-angiotensin system (RAS): vasoconstrictor angiotensin-converting enzyme (ACE)/angiotensin II (ANG II)/ANG II type 1 receptor (AT₁) axis, and vasodilator ACE type 2 (ACE2)/angiotensin 1-7 (ANG 1-7)/Mas receptor axis, in the development of hypoxic pulmonary hypertension in Ren-2 transgenic rats (TGR). Transgene-negative Hannover Sprague-Dawley (HanSD) rats served as controls. Both TGR and HanSD rats responded to two weeks´ exposure to hypoxia with a significant increase in mean pulmonary arterial pressure (MPAP), however, the increase was much less pronounced in the former. The attenuation of hypoxic pulmonary hypertension in TGR as compared to HanSD rats was associated with inhibition of ACE gene expression and activity, inhibition of AT₁receptor gene expression and suppression of ANG II levels in lung tissue. Simultaneously, there was an increase in lung ACE2 gene expression and activity and, in particular, ANG 1-7 concentrations and Mas receptor gene expression. We propose that a combination of suppression of ACE/ANG II/AT₁receptor axis and activation of ACE2/ANG 1-7/Mas receptor axis of the RAS in the lung tissue is the main mechanism explaining attenuation of hypoxic pulmonary hypertension in TGR as compared with HanSD rats.
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