ArticleThe Journal of pharmacology and experimental therapeutics2011
NADPH oxidase pathway is involved in aortic contraction induced by A3 adenosine receptor in mice.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Adenosine AInternational journal of molecular sciences · 2024Review
- Review
- CD73Journal of extracellular vesicles · 2020Article
- Purinergic Signaling During Hyperglycemia in Vascular Smooth Muscle Cells.Frontiers in endocrinology · 2020Review
- Functional changes in vascular reactivity to adenosine receptor activation in type I diabetic mice.European journal of pharmacology · 2018Article
- ROS-dependent activation of RhoA/Rho-kinase in pulmonary artery: Role of Src-family kinases and ARHGEF1.Free radical biology & medicine · 2017Article
- Role of Adenosine Receptor(s) in the Control of Vascular Tone in the Mouse Pudendal Artery.The Journal of pharmacology and experimental therapeutics · 2016Article
- Adenosine A3 Receptor: A promising therapeutic target in cardiovascular disease.Current cardiology reviews · 2016Review
- Control of vascular smooth muscle function by Src-family kinases and reactive oxygen species in health and disease.The Journal of physiology · 2015Review
- Involvement of NADPH oxidase in A2A adenosine receptor-mediated increase in coronary flow in isolated mouse hearts.Purinergic signalling · 2015Article
- A₁ adenosine receptor deficiency or inhibition reduces atherosclerotic lesions in apolipoprotein E deficient mice.Cardiovascular research · 2014Article
- Effects of N-acetylcysteine on isolated mouse skeletal muscle: contractile properties, temperature dependence, and metabolism.Pflugers Archiv : European journal of physiology · 2014Article
- A1 adenosine receptor negatively modulates coronary reactive hyperemia via counteracting A2A-mediated H2O2 production and KATP opening in isolated mouse hearts.American journal of physiology. Heart and circulatory physiology · 2013Article
- Evidence for the involvement of NADPH oxidase in adenosine receptors-mediated control of coronary flow using APhysiological reports · 2013Article
- Interactions between A(2A) adenosine receptors, hydrogen peroxide, and KATP channels in coronary reactive hyperemia.American journal of physiology. Heart and circulatory physiology · 2013Article
- Enhanced depolarization-induced pulmonary vasoconstriction following chronic hypoxia requires EGFR-dependent activation of NAD(P)H oxidase 2.Antioxidants & redox signaling · 2013Article
- Decreased STAT5 phosphorylation and GATA-3 expression in NOX2-deficient T cells: role in T helper development.European journal of immunology · 2012Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The NADPH oxidase (Nox) subunits 1, 2 (gp91 phox), and 4 are the major sources for reactive oxygen species (ROS) in vascular tissues. In conditions such as ischemia-reperfusion and hypoxia, both ROS and adenosine are released, suggesting a possible interaction. Our aim in this study was to examine the A(3) adenosine receptor (A(3)AR)-induced vascular effects and its relation to ROS and Nox1, 2, and 4 using aortic tissues from wild-type (WT) and A(3)AR knockout (A(3)KO) mice. The selective A(3)AR agonist 2-chloro-N(6)-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IBMECA) (10(-10)-10(-5) M) induced contraction of the aorta from WT but not from A(3)KO mice, and this contraction was inhibited by the Nox inhibitor apocynin (10(-5) M) and the ROS scavengers superoxide dismutase-polyethylene glycol and catalase-polyethylene glycol (100 U/ml each). Cl-IBMECA-induced contraction was not affected by the mast cell degranulator compound 48/80 (100 μg/ml) or the stabilizer cromolyn sodium (10(-4) M). In addition, Cl-IBMECA (10(-7) M) increased intracellular ROS generation by 35 ± 14% in WT but not in A(3)KO aorta, and this increase was inhibited by apocynin (10(-5) M), diphenyleneiodonium chloride (10(-5) M), and the A(3)AR antagonist 3-propyl-6-ethyl-5-[(ethylthio)carbonyl]-2 phenyl-4-propyl-3-pyridine carboxylate (MRS1523) (10(-5) M). Furthermore, Cl-IBMECA selectively increased the protein expression of the Nox2 subunit by 150 ± 15% in WT but not in A(3)KO mice without affecting either Nox1 or 4, and this increase was inhibited by apocynin. The mRNA of Nox2 was unchanged by Cl-IBMECA in either WT or A(3)KO aortas. In conclusion, A(3)AR enhances ROS generation, possibly through activation of Nox2, with subsequent contraction of the mouse aorta.
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