ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Arginase 1 contributes to diminished coronary arteriolar dilation in patients with diabetes.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 87 citations in OpenAlex.
- Citrulline Supplementation Improves Microvascular Function and Muscle Strength in Middle-Aged and Older Adults with Type 2 Diabetes.Nutrients · 2025Trial
- Trial
- Serum Argininosuccinic Acid Is Associated with Diabetes in Patients with Coronary Artery Disease: An Exploratory Targeted LC-MS/MS Study.International journal of molecular sciences · 2026Article
- Loss of erythrocyte arginase-1 impairs vasorelaxation due to endothelial GSNOR overexpression and denitrosylation of G protein subunits.Redox biology · 2026Article
- Arginase 1 genetic variation is associated with the risk of vascular complications in type 2 diabetes.Biomarkers in medicine · 2025Article
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Endothelial dysfunction due to eNOS uncoupling: molecular mechanisms as potential therapeutic targets.Cellular & molecular biology letters · 2023Article
- Methylglyoxal-Modified Albumin Effects on Endothelial Arginase Enzyme and Vascular Function.Cells · 2023Article
- Chronic anemia is associated with systemic endothelial dysfunction.Frontiers in cardiovascular medicine · 2023Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Virtual Screening for FDA-Approved Drugs That Selectively Inhibit Arginase Type 1 and 2.Molecules (Basel, Switzerland) · 2022Article
- Association of cerebral microvascular dysfunction and white matter injury in Alzheimer's disease.GeroScience · 2022Article
- Mechanisms and clinical implications of endothelium-dependent vasomotor dysfunction in coronary microvasculature.American journal of physiology. Heart and circulatory physiology · 2022Review
- Elevated serum extracellular vesicle arginase 1 in type 2 diabetes mellitus: a cross-sectional study in middle-aged and elderly population.BMC endocrine disorders · 2022Article
- Beyond eNOS: Genetic influence in NO pathway affecting drug response.Genetics and molecular biology · 2022Article
- Arginase: Biological and Therapeutic Implications in Diabetes Mellitus and Its Complications.Oxidative medicine and cellular longevity · 2022Review
- Novel Therapeutics for Diabetic Retinopathy and Diabetic Macular Edema: A Pathophysiologic Perspective.Frontiers in physiology · 2022Review
- Role of Caveolae in the Development of Microvascular Dysfunction and Hyperglycemia in Type 2 Diabetes.Frontiers in physiology · 2022Article
- Article
- Endothelial Dysfunction: A Contributor to Adverse Cardiovascular Remodeling and Heart Failure Development in Type 2 Diabetes beyond Accelerated Atherogenesis.Journal of clinical medicine · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Arginase 1, via competing with nitric oxide (NO) synthase for the substrate L-arginine, may interfere with NO-mediated vascular responses. We tested the hypothesis that arginase 1 contributes to coronary vasomotor dysfunction in patients with diabetes mellitus (DM). Coronary arterioles were dissected from the right atrial appendages of 41 consecutive patients with or without DM (the 2 groups suffered from similar comorbidities), and agonist-induced changes in diameter were measured with videomicroscopy. We found that the endothelium-dependent agonist ACh elicited a diminished vasodilation and caused constriction to the highest ACh concentration (0.1 μM) with a similar magnitude in patients with (18 ± 8%) and without (17 ± 9%) DM. Responses to ACh were not significantly affected by the inhibition of NO synthesis with N(G)-nitro-L-arginine methyl ester in either group. The NO donor sodium nitroprusside-dependent dilations were not different in patients with or without DM. Interestingly, we found that the presence of N(G)-hydroxy-L-arginine (10 μM), a selective inhibitor of arginase or application of L-arginine (3 mM), restored ACh-induced coronary dilations only in patients with DM (to 47 ± 6% and to 40 ± 19%, respectively) but not in subjects without DM. Correspondingly, the protein expression of arginase 1 was increased in coronary arterioles of patients with DM compared with subjects without diabetes. Moreover, using immunocytochemistry, we detected an abundant immunostaining of arginase 1 in coronary endothelial cells of patients with DM, which was colocalized with NO synthase. Collectively, we provided evidence for a distinct upregulation of arginase 1 in coronary arterioles of patients with DM, which contributes to a reduced NO production and consequently diminished vasodilation.
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