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- W240048233 abstract "We hypothesize that A2A-adenosine receptor (A2A AR)-mediated relaxation is caused by CYP2C generated metabolites whereas, lack of A2A AR promotes contraction via CYP4A in mouse aorta. We measured EETs and DHETs in A2A AR+/+ /A2A AR−/− aorta. DHETs were significantly higher in A2A AR+/+ vs. A2A AR−/− aorta (14,15-DHET: 1.66±0.25 vs. 0.83±0.17; 11,12-DHET: 1.39±0.20 vs. 0.84±0.12; 8,9-DHET: 0.89±0.15 vs. 0.35±0.08 pmol/mg/min p<0.05). No significant differences were observed in EET levels in A2A AR+/+ vs. A2A AR−/− aorta. CYP2C29 was higher in A2A AR+/+ aorta (p<0.05) while CYP4A was higher in A2A AR−/− aorta (p<0.05). CYP2C inhibitor, 1-ABT (5μM) changed the response to NECA (10-6M) from relaxation (+33.99±4.70%) to contraction (25.70±4.75%, p<0.05) in A2A AR+/+. Similar results were obtained in A2A AR+/+ to NECA at 10-6 M with selective CYP2C inhibitor MS-PPOH (10μM, 22.74±5.11%, p<0.05). 1-ABT also changed the response of CGS 21680 (10-6M) from relaxation (+28.44±4.36%) to contraction (18.60±4.66%, p<0.05) in A2A AR+/+. In contrast, no effect was seen in A2A AR−/− with 1-ABT and MS-PPOH. MS-PPOH also caused contraction to CGS 21680 at 10-6M (−18.54±6.06%, p<0.05) in A2A AR+/+, while 1-ABT and MS-PPOH were without an effect in A2A AR−/−. The data show that CYP2C generated metabolites play an important role in A2A AR-mediated relaxation, whereas, in A2A AR−/−, CYP4A induces contraction. Supported by HL027339, GM31278, NIEHS, NS052315, S10RR023461, S10RR023461 & NS052315." @default.
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- W240048233 date "2008-03-01" @default.
- W240048233 modified "2023-10-04" @default.
- W240048233 title "Role of CYP2C generated metabolites in adenosine‐mediated relaxation using A2A AR−/− mice" @default.
- W240048233 doi "https://doi.org/10.1096/fasebj.22.1_supplement.964.23" @default.
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