Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats
Objectives: To explore the role of the renin–angiotensin–aldosterone system (RAAS) in the pathogenesis of pulmonary arterial hypertension (PAH) induced by chronic exposure to cigarette smoke. Methods: 48 healthy male SD rats were randomly divided into four groups (12/group): control group (group A);...
Main Authors: | , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
SAGE Publications
2015-06-01
|
Series: | Journal of the Renin-Angiotensin-Aldosterone System |
Online Access: | https://doi.org/10.1177/1470320315576256 |
_version_ | 1797282083506225152 |
---|---|
author | Yi-Ming Yuan Li Luo Zhen Guo Ming Yang Ren-Song Ye Chuan Luo |
author_facet | Yi-Ming Yuan Li Luo Zhen Guo Ming Yang Ren-Song Ye Chuan Luo |
author_sort | Yi-Ming Yuan |
collection | DOAJ |
description | Objectives: To explore the role of the renin–angiotensin–aldosterone system (RAAS) in the pathogenesis of pulmonary arterial hypertension (PAH) induced by chronic exposure to cigarette smoke. Methods: 48 healthy male SD rats were randomly divided into four groups (12/group): control group (group A); inhibitor alone group (group B); cigarette induction group (group C); cigarette induction + inhibitor group (group D). After the establishment of smoking-induced PAH rat model, the right ventricular systolic pressure (RVSP) was detected using an inserted catheter; western blotting was used to detect the protein expression of angiotensin-converting enzyme-2 (ACE2) and angiotensin-converting enzyme (ACE); expression levels of angiotensin II (AngII) in lung tissue were measured by radioimmunoassay. Results: After six months of cigarette exposure, the RVSP of chronic cigarette induction group was significantly higher than that of the control group; expression levels of AngII and ACE increased in lung tissues, but ACE2 expression levels reduced. Compared with cigarette exposure group, after losartan treatment, RVSP, ACE and AngII obviously decreased ( P <0.05), and ACE2 expression levels significantly increased. Conclusion: Chronic cigarette exposure may result in PAH and affect the protein expression of ACE2 and ACE in lung tissue, suggesting that ACE2 and ACE play an important role in the pathogenesis of smoking-induced PAH. |
first_indexed | 2024-03-07T17:06:51Z |
format | Article |
id | doaj.art-6b6b9b1abe2644b3833c0d8586d62cec |
institution | Directory Open Access Journal |
issn | 1470-3203 1752-8976 |
language | English |
last_indexed | 2024-03-07T17:06:51Z |
publishDate | 2015-06-01 |
publisher | SAGE Publications |
record_format | Article |
series | Journal of the Renin-Angiotensin-Aldosterone System |
spelling | doaj.art-6b6b9b1abe2644b3833c0d8586d62cec2024-03-03T02:33:08ZengSAGE PublicationsJournal of the Renin-Angiotensin-Aldosterone System1470-32031752-89762015-06-011610.1177/1470320315576256Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) ratsYi-Ming Yuan0Li Luo1Zhen Guo2Ming Yang3Ren-Song Ye4Chuan Luo5Department of Geriatric Medicine, West China Hospital, Sichuan University, ChinaDepartment of Geriatric Medicine, West China Hospital, Sichuan University, ChinaENT Department, Pixian TCM Hospital, ChinaDepartment of Geriatric Medicine, West China Hospital, Sichuan University, ChinaDepartment of Internal Medicine, The Affiliated Shanghai Eighth People’s Hospital of Jiangsu University,Shanghai, ChinaDepartment of Geriatric Medicine, West China Hospital, Sichuan University, ChinaObjectives: To explore the role of the renin–angiotensin–aldosterone system (RAAS) in the pathogenesis of pulmonary arterial hypertension (PAH) induced by chronic exposure to cigarette smoke. Methods: 48 healthy male SD rats were randomly divided into four groups (12/group): control group (group A); inhibitor alone group (group B); cigarette induction group (group C); cigarette induction + inhibitor group (group D). After the establishment of smoking-induced PAH rat model, the right ventricular systolic pressure (RVSP) was detected using an inserted catheter; western blotting was used to detect the protein expression of angiotensin-converting enzyme-2 (ACE2) and angiotensin-converting enzyme (ACE); expression levels of angiotensin II (AngII) in lung tissue were measured by radioimmunoassay. Results: After six months of cigarette exposure, the RVSP of chronic cigarette induction group was significantly higher than that of the control group; expression levels of AngII and ACE increased in lung tissues, but ACE2 expression levels reduced. Compared with cigarette exposure group, after losartan treatment, RVSP, ACE and AngII obviously decreased ( P <0.05), and ACE2 expression levels significantly increased. Conclusion: Chronic cigarette exposure may result in PAH and affect the protein expression of ACE2 and ACE in lung tissue, suggesting that ACE2 and ACE play an important role in the pathogenesis of smoking-induced PAH.https://doi.org/10.1177/1470320315576256 |
spellingShingle | Yi-Ming Yuan Li Luo Zhen Guo Ming Yang Ren-Song Ye Chuan Luo Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats Journal of the Renin-Angiotensin-Aldosterone System |
title | Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats |
title_full | Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats |
title_fullStr | Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats |
title_full_unstemmed | Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats |
title_short | Activation of renin–angiotensin–aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats |
title_sort | activation of renin angiotensin aldosterone system raas in the lung of smoking induced pulmonary arterial hypertension pah rats |
url | https://doi.org/10.1177/1470320315576256 |
work_keys_str_mv | AT yimingyuan activationofreninangiotensinaldosteronesystemraasinthelungofsmokinginducedpulmonaryarterialhypertensionpahrats AT liluo activationofreninangiotensinaldosteronesystemraasinthelungofsmokinginducedpulmonaryarterialhypertensionpahrats AT zhenguo activationofreninangiotensinaldosteronesystemraasinthelungofsmokinginducedpulmonaryarterialhypertensionpahrats AT mingyang activationofreninangiotensinaldosteronesystemraasinthelungofsmokinginducedpulmonaryarterialhypertensionpahrats AT rensongye activationofreninangiotensinaldosteronesystemraasinthelungofsmokinginducedpulmonaryarterialhypertensionpahrats AT chuanluo activationofreninangiotensinaldosteronesystemraasinthelungofsmokinginducedpulmonaryarterialhypertensionpahrats |