ArticleThe Journal of experimental medicine2009
Angiotensin II impairs endothelial function via tyrosine phosphorylation of the endothelial nitric oxide synthase.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 141 citations in OpenAlex.
- Endothelial nitric oxide signaling in cellular and systemic metabolism.Redox biology · 2026Review
- G-Protein-Coupled Receptors in Chronic Kidney Disease Induced by Hypertension and Diabetes.Cells · 2025Review
- The Ever-Expanding Influence of the Endothelial Nitric Oxide Synthase.Basic & clinical pharmacology & toxicology · 2025Review
- Noise causes cardiovascular disease: it's time to act.Journal of exposure science & environmental epidemiology · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Immune and Metabolic Mechanisms of Endothelial Dysfunction.International journal of molecular sciences · 2024Review
- Angiotensin II Directly Increases Endothelial Calcium and Nitric Oxide in Kidney and Brain Microvessels In Vivo With Reduced Efficacy in Hypertension.Journal of the American Heart Association · 2024Article
- Hypertension, Neurodegeneration, and Cognitive Decline.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Health position paper and redox perspectives - Disease burden by transportation noise.Redox biology · 2024Review
- E-cigarette effects on vascular function in animals and humans.Pflugers Archiv : European journal of physiology · 2023Review
- Vascular Redox Signaling, Endothelial Nitric Oxide Synthase Uncoupling, and Endothelial Dysfunction in the Setting of Transportation Noise Exposure or Chronic Treatment with Organic Nitrates.Antioxidants & redox signaling · 2023Review
- YAP-galectin-3 signaling mediates endothelial dysfunction in angiotensin II-induced hypertension in mice.Cellular and molecular life sciences : CMLS · 2023Article
- The Effects of Acidosis on eNOS in the Systemic Vasculature: A Focus on Early Postnatal Ontogenesis.International journal of molecular sciences · 2022Review
- Nitric Oxide as a Central Molecule in Hypertension: Focus on the Vasorelaxant Activity of New Nitric Oxide Donors.Biology · 2021Review
- Endothelial-transcytosed myeloperoxidase activates endothelial nitric oxide synthase via a phospholipase C-dependent calcium signaling pathway.Free radical biology & medicine · 2021Article
- A review on SARS-CoV-2 and stroke pathogenesis and outcome.The Egyptian journal of neurology, psychiatry and neurosurgery · 2021Review
- Redox Switches in Noise-Induced Cardiovascular and Neuronal Dysregulation.Frontiers in molecular biosciences · 2021Review
- Nitric Oxide Synthase Inhibitors into the Clinic at Last.Handbook of experimental pharmacology · 2021Article
- Effects of different enantiomers of amlodipine on lipid profiles and vasomotor factors in atherosclerotic rabbits.Open life sciences · 2021Article
- ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proline-rich tyrosine kinase 2 (PYK2) can be activated by angiotensin II (Ang II) and reactive oxygen species. We report that in endothelial cells, Ang II enhances the tyrosine phosphorylation of endothelial NO synthase (eNOS) in an AT(1)-, H(2)O(2)-, and PYK2-dependent manner. Low concentrations (1-100 micromol/liter) of H(2)O(2) stimulated the phosphorylation of eNOS Tyr657 without affecting that of Ser1177, and attenuated basal and agonist-induced NO production. In isolated mouse aortae, 30 micromol/liter H(2)O(2) induced phosphorylation of eNOS on Tyr657 and impaired acetylcholine-induced relaxation. Endothelial overexpression of a dominant-negative PYK2 mutant protected against H(2)O(2)-induced endothelial dysfunction. Correspondingly, carotid arteries from eNOS(-/-) mice overexpressing the nonphosphorylatable eNOS Y657F mutant were also protected against H(2)O(2). In vivo, 3 wk of treatment with Ang II considerably increased levels of Tyr657-phosphorylated eNOS in the aortae of wild-type but not Nox2(y/-) mice, and this was again associated with a clear impairment in endothelium-dependent vasodilatation in the wild-type but not in the Nox2(y/-) mice. Collectively, endothelial PYK2 activation by Ang II and H(2)O(2) causes the phosphorylation of eNOS on Tyr657, attenuating NO production and endothelium-dependent vasodilatation. This mechanism may contribute to the endothelial dysfunction observed in cardiovascular diseases associated with increased activity of the renin-angiotensin system and elevated redox stress.
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