Adenosine A2A receptor and vascular response: role of soluble epoxide hydrolase, adenosine A1 receptor and angiotensin-II

Previously, we have reported that the coronary reactive hyperemic response was reduced in adenosine A2A receptor-null (A2AAR?/?) mice, and it reversed by soluble epoxide hydrolase (sEH) inhibitor. However, is unknown aortic vascular response, therefore, hypothesized A2AAR-gene deletion mice affects adenosine-induced increase sEH A1 receptor (A1AR) activities. A2AAR?/? showed an sEH, AI AR CYP450-4A protein expression but decrease CYP450-2C compared to C57Bl/6 mice. NECA (adenosine-analog) CCPA (adenosine receptor-agonist)-induced dose-dependent tested with t-AUCB (sEH-inhibitor) angiotensin-II (Ang-II) vs. In A2AAR?/?, CCPA-induced vasoconstriction contraction NECA. Similarly, CCPA. addition, Ang-II enhanced also Further, Ang-II-enhanced Our data suggest depends on A1AR CYP4A expression.