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The pulmonary renin-angiotensin system
1Centre for Respiratory Research, Royal Free and University College London Medical School, Rayne Institute, UK. richard.marshall@ucl.ac.uk
Current Pharmaceutical Design
|February 7, 2003
Summary
A local pulmonary renin-angiotensin system (RAS) may drive lung injury and repair. Therapies targeting this system show promise for treating diffuse parenchymal lung diseases.
Area of Science:
- Pulmonary Medicine
- Cardiovascular Physiology
- Cellular Biology
Background:
- The circulating renin-angiotensin system (RAS) regulates homeostasis.
- Local tissue-based RAS are implicated in injury and repair processes.
- Evidence suggests a pulmonary RAS exists in interstitial lung diseases.
Purpose of the Study:
- To investigate the role of a pulmonary RAS in lung injury and repair.
- To explore the potential therapeutic applications of RAS inhibitors in diffuse parenchymal lung disease.
Main Methods:
- Analysis of RAS component expression in lung tissue.
- Assessment of angiotensin-converting enzyme (ACE) levels in interstitial lung diseases.
- Evaluation of ACE inhibitors and angiotensin II receptor antagonists in experimental lung injury models.
Main Results:
- Expression of RAS components and elevated ACE suggest a pulmonary RAS.
- Angiotensin II may mediate lung injury responses via increased vascular permeability, vascular tone, fibroblast activity, and reduced epithelial cell survival.
- ACE inhibitors and angiotensin II receptor antagonists attenuated experimental lung injury.
Conclusions:
- Activation of a local pulmonary RAS contributes to lung injury pathogenesis.
- RAS-targeting agents may be beneficial for treating diffuse parenchymal lung disease.
- Further research is needed to identify specific cell types and effector molecules involved in pulmonary RAS.