ArticleFrontiers in immunology2013
Arginase 1 mediates increased blood pressure and contributes to vascular endothelial dysfunction in deoxycorticosterone acetate-salt hypertension.
Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- ARG1-polyamine axis: cell-type-specific functions in disease pathogenesis and therapeutic targeting.Frontiers in immunology · 2026Review
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Genetic deletion of 12/15 lipoxygenase delays vascular remodeling and limits cardiorenal dysfunction after pressure overload.Journal of molecular and cellular cardiology plus · 2023Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Virus-Induced Membrane Fusion in Neurodegenerative Disorders.Frontiers in cellular and infection microbiology · 2022Review
- Transforming growth factor-beta and liver injury in an arginine vasopressin-induced pregnant rat model.Clinical and experimental reproductive medicine · 2021Article
- Norvaline Reduces Blood Pressure and Induces Diuresis in Rats with Inherited Stress-Induced Arterial Hypertension.BioMed research international · 2020Article
- Article
- L-arginase induces vascular dysfunction in old spontaneously hypertensive rats.Journal of African Association of Physiological Sciences · 2019Article
- Increased Vascular Contractility in Hypertension Results From Impaired Endothelial Calcium Signaling.Hypertension (Dallas, Tex. : 1979) · 2019Article
- The role of psychosocial determinants in predicting adherence to treatment in patient with hypertension.Interventional medicine & applied science · 2019Article
- Age-Dependent Oxidative Stress Elevates Arginase 1 and Uncoupled Nitric Oxide Synthesis in Skeletal Muscle of Aged Mice.Oxidative medicine and cellular longevity · 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
- Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Coronary microvascular disease as an early culprit in the pathophysiology of diabetes and metabolic syndrome.Pharmacological research · 2017Review
- NOX2-Induced Activation of Arginase and Diabetes-Induced Retinal Endothelial Cell Senescence.Antioxidants (Basel, Switzerland) · 2017Article
- Endothelial Mineralocorticoid Receptor Mediates Diet-Induced Aortic Stiffness in Females.Circulation research · 2016Article
- Neuropathy optic glaucomatosa induced by systemic hypertension through activation endothelin-1 signaling pathway in central retinal artery in rats.International journal of ophthalmology · 2016Article
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10 authors at 1 institution in 1 country.
Funding
Abstract
Enhanced arginase (ARG) activity has been identified as a factor that reduces nitric oxide production and impairs endothelial function in vascular pathologies. Using a gene deletion model, we investigated involvement of arginase isoforms arginase 1 and 2 (ARG1 and ARG2) in hypertension and endothelial dysfunction in a mineralocorticoid-salt mouse model. Hypertension was induced in wild type (WT), partial ARG1(+/-) knockout (KO), and complete ARG2(-/-) KO mice by uninephrectomy and deoxycorticosterone acetate (DOCA)-salt treatment for 6-weeks. (Control uninephrectomized mice drank tap water.) After 2 weeks of DOCA-salt treatment, systolic blood pressure (SBP) was increased by ∼15 mmHg in all mouse genotypes. SBP continued to rise in DOCA-salt WT and ARG2(-/-) mice to ∼130 mmHg at 5-6 weeks, whereas in ARG1(+/-) mice SBP waned toward control levels by 6 weeks (109 ± 4 vs. 101 ± 3 mmHg, respectively). DOCA-salt treatment in WT mice increased vascular ARG activity (aorta by 1.5-fold; mesenteric artery (MA) by 2.6-fold and protein levels of ARG1 (aorta: 1.49-fold and MA: 1.73-fold) vs. WT Sham tissues. ARG2 protein increased in WT-DOCA MA (by 2.15-fold) but not in aorta compared to those of WT Sham tissues. Maximum endothelium-dependent vasorelaxation to acetylcholine was significantly reduced in DOCA-salt WT mice and largely or partially maintained in DOCA ARG1(+/-) and ARG2(-/-) mice vs. their Sham controls. DOCA-salt augmented contractile responses to phenylephrine in aorta of all mouse genotypes. Additionally, treatment of aorta or MA from WT-DOCA mice with arginase inhibitor (100 μM) improved endothelium-mediated vasorelaxation. DOCA-salt-induced coronary perivascular fibrosis (increased by 2.1-fold) in WT was prevented in ARG1(+/-) and reduced in ARG2(-/-) mice. In summary, ARG is involved in murine DOCA-salt-induced impairment of vascular function and hypertension and may represent a novel target for antihypertensive therapy.
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