ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Agonists of MAS oncogene and angiotensin II type 2 receptors attenuate cardiopulmonary disease in rats with neonatal hyperoxia-induced lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 93 citations in OpenAlex.
- Tailoring Therapy to Bronchopulmonary Dysplasia Phenotype: A Ten-Year Experience in Precision Medicine.Children (Basel, Switzerland) · 2026Article
- Diagnostic and therapeutic precision in cardiovascular diseases in the neonatal intensive care.Journal of perinatology : official journal of the California Perinatal Association · 2025Review
- Angiotensin II Type 2 Receptor Inhibits M1 Polarization and Apoptosis of Alveolar Macrophage and Protects Against Mechanical Ventilation-Induced Lung Injury.Inflammation · 2025Article
- Systemic hemodynamics and pediatric lung disease: mechanistic links and therapeutic relevance.American journal of physiology. Heart and circulatory physiology · 2024Review
- Effects of the Oral Angiotensin II Type 2 Receptor Agonist C21 in Sugen-Hypoxia Induced Pulmonary Hypertension in Rats.International journal of molecular sciences · 2023Article
- Circular RNAs expression profiles and bioinformatics analysis in bronchopulmonary dysplasia.Journal of clinical laboratory analysis · 2023Article
- Targeting vasculature to reduce fetal growth restriction associated bronchopulmonary dysplasia.Respirology (Carlton, Vic.) · 2022Article
- The Angiotensin ATPharmacological reviews · 2022Review
- Review
- Hypertension in chronic kidney disease: What lies behind the scene.Frontiers in pharmacology · 2022Review
- Classical and Counter-Regulatory Renin-Angiotensin System: Potential Key Roles in COVID-19 Pathophysiology.CJC open · 2021Review
- Angiotensin II Type 2 Receptor: A Target for Protection Against Hypertension, Metabolic Dysfunction, and Organ Remodeling.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Developing new drugs that activate the protective arm of the renin-angiotensin system as a potential treatment for respiratory failure in COVID-19 patients.Drug discovery today · 2021Review
- The Tissue Renin-Angiotensin System and Its Role in the Pathogenesis of Major Human Diseases: Quo Vadis?Cells · 2021Review
- ACE2/Ang-(1-7)/Mas1 axis and the vascular system: vasoprotection to COVID-19-associated vascular disease.Clinical science (London, England : 1979) · 2021Review
- Regulation of ACE-2 enzyme by hyperoxia in lung epithelial cells by post-translational modification.Journal of lung, pulmonary & respiratory research · 2021Article
- Angiotensin Converting Enzyme-2 (ACE-2) role in disease and future in research.Journal of lung, pulmonary & respiratory research · 2021Article
- Biosynthesis of lanthionine-constrained agonists of G protein-coupled receptors.Biochemical Society transactions · 2020Review
- Use of Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers During the COVID-19 Pandemic: A Modeling Analysis.PLoS computational biology · 2020Article
- Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Stimulation of MAS oncogene receptor (MAS) or angiotensin (Ang) receptor type 2 (AT2) may be novel therapeutic options for neonatal chronic lung disease (CLD) by counterbalancing the adverse effects of the potent vasoconstrictor angiotensin II, consisting of arterial hypertension (PAH)-induced right ventricular hypertrophy (RVH) and pulmonary inflammation. We determined the cardiopulmonary effects in neonatal rats with CLD of daily treatment during continuous exposure to 100% oxygen for 10 days with specific ligands for MAS [cyclic Ang-(1-7); 10-50 μg·kg(-1)·day(-1)] and AT2 [dKcAng-(1-7); 5-20 μg·kg(-1)·day(-1)]. Parameters investigated included lung and heart histopathology, fibrin deposition, vascular leakage, and differential mRNA expression in the lungs of key genes involved in the renin-angiotensin system, inflammation, coagulation, and alveolar development. We investigated the role of nitric oxide synthase inhibition with N(ω)-nitro-l-arginine methyl ester (25 mg·kg(-1)·day(-1)) during AT2 agonist treatment. Prophylactic treatment with agonists for MAS or AT2 for 10 days diminished cardiopulmonary injury by reducing alveolar septum thickness and medial wall thickness of small arterioles and preventing RVH. Both agonists attenuated the pulmonary influx of inflammatory cells, including macrophages (via AT2) and neutrophils (via MAS) but did not reduce alveolar enlargement and vascular alveolar leakage. The AT2 agonist attenuated hyperoxia-induced fibrin deposition. In conclusion, stimulation of MAS or AT2 attenuates cardiopulmonary injury by reducing pulmonary inflammation and preventing PAH-induced RVH but does not affect alveolar and vascular development in neonatal rats with experimental CLD. The beneficial effects of AT2 activation on experimental CLD were mediated via a NOS-independent mechanism.
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