ArticleThe journal of sexual medicine2011
Arginase II deletion increases corpora cavernosa relaxation in diabetic mice.
Article in The journal of sexual medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 65 citations in OpenAlex.
- Erectile Dysfunction in Diabetes Mellitus: A Comprehensive Narrative Review of Pathophysiology, Genetic Association Studies and Therapeutic Approaches.Endocrinology, diabetes & metabolism · 2025Review
- Animal models in the study of diabetic erectile dysfunction: mechanisms and applications.Frontiers in endocrinology · 2025Review
- Arginase: Biological and Therapeutic Implications in Diabetes Mellitus and Its Complications.Oxidative medicine and cellular longevity · 2022Review
- Traditional chinese medicine to prevent and treat diabetic erectile dysfunction.Frontiers in pharmacology · 2022Review
- Is the Arginase Pathway a Novel Therapeutic Avenue for Diabetic Retinopathy?Journal of clinical medicine · 2020Review
- Hyperglycemia-impaired aortic vasorelaxation mediated through arginase elevation: Role of stress kinase pathways.European journal of pharmacology · 2019Article
- Deficient arginase II expression without alteration in arginase I expression attenuated experimental autoimmune encephalomyelitis in mice.Immunology · 2018Article
- Deletion of endothelial arginase 1 does not improve vasomotor function in diabetic mice.Physiological reports · 2018Article
- Arginase: A Multifaceted Enzyme Important in Health and Disease.Physiological reviews · 2018Review
- Supplementation with Phycocyanobilin, Citrulline, Taurine, and Supranutritional Doses of Folic Acid and Biotin-Potential for Preventing or Slowing the Progression of Diabetic Complications.Healthcare (Basel, Switzerland) · 2017Article
- Endothelin-1 Overexpression Exaggerates Diabetes-Induced Endothelial Dysfunction by Altering Oxidative Stress.American journal of hypertension · 2016Article
- Arginase: an old enzyme with new tricks.Trends in pharmacological sciences · 2015Review
- Gas what: NO is not the only answer to sexual function.British journal of pharmacology · 2015Review
- Angiotensin II-induced arterial thickening, fibrosis and stiffening involves elevated arginase function.PloS one · 2015Article
- Arginase in retinopathy.Progress in retinal and eye research · 2013Review
- Activated Rho kinase mediates diabetes-induced elevation of vascular arginase activation and contributes to impaired corpora cavernosa relaxation: possible involvement of p38 MAPK activation.The journal of sexual medicine · 2013Article
- Prevention of diabetes-induced arginase activation and vascular dysfunction by Rho kinase (ROCK) knockout.Cardiovascular research · 2013Article
- The role of arginase I in diabetes-induced retinal vascular dysfunction in mouse and rat models of diabetes.Diabetologia · 2013Article
- Vasomotor regulation of coronary microcirculation by oxidative stress: role of arginase.Frontiers in immunology · 2013Article
- Arginase promotes skeletal muscle arteriolar endothelial dysfunction in diabetic rats.Frontiers in immunology · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
introductionDiabetes-induced erectile dysfunction involves elevated arginase (Arg) activity and expression. Because nitric oxide (NO) synthase and Arg share and compete for their substrate L-arginine, NO production is likely linked to regulation of Arg. Arg is highly expressed and implicated in erectile dysfunction.
aimIt was hypothesized that Arg-II isoform deletion enhances relaxation function of corpora cavernosal (CC) smooth muscle in a streptozotocin (STZ) diabetic model.
methodsEight weeks after STZ-induced diabetes, vascular functional studies, Arg activity assay, and protein expression levels of Arg and constitutive NOS (using Western blots) were assessed in CC tissues from nondiabetic wild type (WT), diabetic (D) WT (WT + D), Arg-II knockout (KO), and Arg-II KO+D mice (N = 8-10 per group).
main outcome measuresInhibition or lack of arginase results in facilitation of CC relaxation in diabetic CC.
resultsStrips of CC from Arg-II KO mice exhibited an enhanced maximum endothelium-dependent relaxation (from 70 + 3% to 84 + 4%) and increased nitrergic relaxation (by 55%, 71%, 42%, 42%, and 24% for 1, 2, 4, 8 and 16 Hz, respectively) compared with WT mice. WT + D mice showed a significant reduction of endothelium-dependent maximum relaxation (44 + 8%), but this impairment of relaxation was significantly prevented in Arg-II KO+D mice (69 + 4%). Sympathetic-mediated and alpha-adrenergic agent-induced contractile responses also were increased in CC strips from D compared with non-D controls. Contractile responses were significantly lower in Arg-II KO control and D versus the WT groups. WT + D mice increased Arg activity (1.5-fold) and Arg-II protein expression and decreased total and phospho-eNOS at Ser-1177, and nNOS levels. These alterations were not seen in Arg-II KO mice. Additionally, the Arg inhibitor BEC (50 µM) enhanced nitrergic and endothelium-dependent relaxation in CC of WT + D mice.
conclusionThese studies show for the first time that Arg-II deletion improves CC relaxation in type 1 diabetes.
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