ArticleAmerican journal of physiology. Cell physiology2011
Angiotensin II-induced vascular endothelial dysfunction through RhoA/Rho kinase/p38 mitogen-activated protein kinase/arginase pathway.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 134 citations in OpenAlex.
- A combination of oral L-citrulline and L-arginine improved 10-min full-power cycling test performance in male collegiate soccer players: a randomized crossover trial.European journal of applied physiology · 2019Trial
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- Advances in immune-inflammatory interactions within the testicular-penile microenvironment of varicocele patients: molecular mechanisms underlying erectile dysfunction and spermatogenic impairment.Frontiers in endocrinology · 2026Review
- Angiotensin II Activates Yes-Associated Protein (YAP) in Fibroblast Promoting Deep Fascia Remodeling.International journal of molecular sciences · 2025Article
- Chronic Copper Overload Triggers Inflammation in Mesenteric PVAT Alongside Changes in Renin-Angiotensin System-Related Pathways.Nutrients · 2025Article
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- Chemokine Fractalkine and Non-Obstructive Coronary Artery Disease-Is There a Link?International journal of molecular sciences · 2024Review
- Role of Angiotensin II in Cardiovascular Diseases: Introducing Bisartans as a Novel Therapy for Coronavirus 2019.Biomolecules · 2023Review
- Methylglyoxal-Modified Albumin Effects on Endothelial Arginase Enzyme and Vascular Function.Cells · 2023Article
- Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023Review
- Lack of adducin impairs the stability of endothelial adherens and tight junctions and may be required for cAMP-Rac1-mediated endothelial barrier stabilization.Scientific reports · 2022Article
- Disparate biomechanical properties of the aorta in non-aneurysmal and aneurysmal mice treated with angiotensin II.Physiological reports · 2022Article
- Angiotensin II type 1 receptor localizes at the blood-bile barrier in humans and pigs.Histochemistry and cell biology · 2022Article
- Functional ACE2 deficiency leading to angiotensin imbalance in the pathophysiology of COVID-19.Reviews in endocrine & metabolic disorders · 2022Review
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- Endothelial MicroRNA-483-3p Is Hypertension-Protective.Oxidative medicine and cellular longevity · 2022Article
- Binding of the Andes Virus Nucleocapsid Protein to RhoGDI Induces the Release and Activation of the Permeability Factor RhoA.Journal of virology · 2021Article
- Persistent Endothelial Dysfunction in Post-Acute COVID-19 Syndrome: A Case-Control Study.Biomedicines · 2021Article
- Role of the Renin-Angiotensin-Aldosterone and Kinin-Kallikrein Systems in the Cardiovascular Complications of COVID-19 and Long COVID.International journal of molecular sciences · 2021Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Enhanced vascular arginase activity impairs endothelium-dependent vasorelaxation by decreasing l-arginine availability to endothelial nitric oxide (NO) synthase, thereby reducing NO production. Elevated angiotensin II (ANG II) is a key component of endothelial dysfunction in many cardiovascular diseases and has been linked to elevated arginase activity. We determined signaling mechanisms by which ANG II increases endothelial arginase function. Results show that ANG II (0.1 μM, 24 h) elevates arginase activity and arginase I expression in bovine aortic endothelial cells (BAECs) and decreases NO production. These effects are prevented by the arginase inhibitor BEC (100 μM). Blockade of ANG II AT(1) receptors or transfection with small interfering RNA (siRNA) for Gα12 and Gα13 also prevents ANG II-induced elevation of arginase activity, but siRNA for Gαq does not. ANG II also elevates active RhoA levels and induces phosphorylation of p38 MAPK. Inhibitors of RhoA activation (simvastatin, 0.1 μM) or Rho kinase (ROCK) (Y-27632, 10 μM; H1152, 0.5 μM) block both ANG II-induced elevation of arginase activity and phosphorylation of p38 MAPK. Furthermore, pretreatment of BAECs with p38 inhibitor SB-202190 (2 μM) or transfection with p38 MAPK siRNA prevents ANG II-induced increased arginase activity/expression and maintains NO production. Additionally, inhibitors of p38 MAPK (SB-203580, 5 μg·kg(-1)·day(-1)) or arginase (ABH, 8 mg·kg(-1)·day(-1)) or arginase gene knockout in mice prevents ANG II-induced vascular endothelial dysfunction and associated enhancement of arginase. These results indicate that ANG II increases endothelial arginase activity/expression through Gα12/13 G proteins coupled to AT(1) receptors and subsequent activation of RhoA/ROCK/p38 MAPK pathways leading to endothelial dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.