ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Role of CYP epoxygenases in A2A AR-mediated relaxation using A2A AR-null and wild-type mice.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
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- Contribution of Adenosine in the Physiological Changes and Injuries Secondary to Exposure to Extreme Oxygen Pressure in Healthy Subjects.Biomedicines · 2022Review
- Adenosine AMolecular and cellular biochemistry · 2021Article
- Ephx2-gene deletion affects acetylcholine-induced relaxation in angiotensin-II infused mice: role of nitric oxide and CYP-epoxygenases.Molecular and cellular biochemistry · 2020Article
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- Role of oxylipins in cardiovascular diseases.Acta pharmacologica Sinica · 2018Review
- Functional changes in vascular reactivity to adenosine receptor activation in type I diabetic mice.European journal of pharmacology · 2018Article
- Exploring Adenosine Receptor Ligands: Potential Role in the Treatment of Cardiovascular Diseases.Molecules (Basel, Switzerland) · 2017Review
- Drug Delivery and Nanoformulations for the Cardiovascular System.Research & reviews. Drug delivery · 2017Article
- The Role of Adenosine ABioMed research international · 2017Review
- Vascular endothelial over-expression of soluble epoxide hydrolase (Tie2-sEH) enhances adenosine AMolecular and cellular biochemistry · 2016Article
- Deletion of soluble epoxide hydrolase enhances coronary reactive hyperemia in isolated mouse heart: role of oxylipins and PPARγ.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Role of Adenosine Receptor(s) in the Control of Vascular Tone in the Mouse Pudendal Artery.The Journal of pharmacology and experimental therapeutics · 2016Article
- Angiotensin II stimulation alters vasomotor response to adenosine in mouse mesenteric artery: role for A1 and A2B adenosine receptors.British journal of pharmacology · 2015Article
- High salt diet exacerbates vascular contraction in the absence of adenosine A₂A receptor.Journal of cardiovascular pharmacology · 2014Article
- Adenosine APhysiological reports · 2013Article
- Adenosine A1 receptors link to smooth muscle contraction via CYP4a, protein kinase C-α, and ERK1/2.Journal of cardiovascular pharmacology · 2013Article
- Adenosine A2A receptor modulates vascular response in soluble epoxide hydrolase-null mice through CYP-epoxygenases and PPARγ.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
We hypothesized that A2A adenosine receptor (A2A AR) activation causes vasorelaxation through cytochrome P-450 (CYP) epoxygenases and endothelium-derived hyperpolarizing factors, whereas lack of A2A AR activation promotes vasoconstriction through Cyp4a in the mouse aorta. Adenosine 5'-N-ethylcarboxamide (NECA; 10(-6) M), an adenosine analog, caused relaxation in wild-type A2A AR (A2A AR+/+; +33.99 +/- 4.70%, P < 0.05) versus contraction in A2A AR knockout (A2A AR(-/-); -27.52 +/- 4.11%) mouse aortae. An A2A AR-specific antagonist (SCH-58261; 1 microM) changed the NECA (10(-6) M) relaxation response to contraction (-35.82 +/- 4.69%, P < 0.05) in A2A AR+/+ aortae, whereas no effect was noted in A2A AR(-/-) aortae. Significant contraction was seen in the absence of the endothelium in A2A AR+/+ (-2.58 +/- 2.25%) aortae compared with endothelium-intact aortae. An endothelial nitric oxide synthase inhibitor (N-nitro-L-arginine methyl ester; 100 microM) and a cyclooxygenase inhibitor (indomethacin; 10 microM) failed to block NECA-induced relaxation in A2A AR+/+ aortae. A selective inhibitor of CYP epoxygenases (methylsulfonyl-propargyloxyphenylhexanamide; 10 microM) changed NECA-mediated relaxation (-22.74 +/- 5.11% at 10(-6) M) and CGS-21680-mediated relaxation (-18.54 +/- 6.06% at 10(-6) M) to contraction in A2A AR+/+ aortae, whereas no response was noted in A2A AR(-/-) aortae. Furthermore, an epoxyeicosatrienoic acid (EET) antagonist [14,15-epoxyeicosa-5(Z)-enoic acid; 10 microM] was able to block NECA-induced relaxation in A2A AR+/+ aortae, whereas omega-hydroxylase inhibitors (10 microM dibromo-dodecenyl-methylsulfimide and 10 microM HET-0016) changed contraction into relaxation in A2A AR(-/-) aorta. Cyp2c29 protein was upregulated in A2A AR+/+ aortae, whereas Cyp4a was upregulated in A2A AR(-/-) aortae. Higher levels of dihydroxyeicosatrienoic acids (DHETs; 14,15-DHET, 11,12-DHET, and 8,9-DHET, P < 0.05) were found in A2A AR+/+ versus A2A AR(-/-) aortae. EET levels were not significantly different between A2A AR+/+ and A2A AR(-/-) aortae. It is concluded that CYP epoxygenases play an important role in A2A AR-mediated relaxation, and the deletion of the A2A AR leads to contraction through Cyp4a.
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