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Am J Physiol Heart Circ Physiol 282: H1206-H1215, 2002; doi:10.1152/ajpheart.00839.2000
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Vol. 282, Issue 4, H1206-H1215, April 2002

AT1 and AT2 receptor expression and blockade after acute ischemia-reperfusion in isolated working rat hearts

Yi Xu1, Dinender Kumar1,2, Jason R. B. Dyck2, William R. Ford1, Alexander S. Clanachan2, Gary D. Lopaschuk2, and Bodh I. Jugdutt1,2

1 Division of Cardiology, Department of Medicine and 2 Cardiovascular Research Group, Faculty of Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2R7

We assessed ANG II type 1 (AT1) and type 2 (AT2) receptor (R) expression and functional recovery after ischemia-reperfusion with or without AT1R/AT2R blockade in isolated working rat hearts. Groups of six hearts were subjected to global ischemia (30 min) followed by reperfusion (30 min) and exposed to no drug and no ischemia-reperfusion (control), ischemia-reperfusion and no drug, and ischemia-reperfusion with losartan (an AT1R antagonist; 1 µmol/l), PD-123319 (an AT2R antagonist; 0.3 µmol/l), N6-cyclohexyladenosine (CHA, a cardioprotective adenosine A1 receptor agonist; 0.5 µmol/l as positive control), enalaprilat (an ANG-converting enzyme inhibitor; 1 µmol/l), PD-123319 + losartan, ANG II (1 nmol/l), or ANG II + losartan. Compared with controls, ischemia-reperfusion decreased AT2R protein (Western immunoblots) and mRNA (Northern immunoblots, RT-PCR) and impaired functional recovery. PD-123319 increased AT2R protein and mRNA and improved functional recovery. Losartan increased AT1R mRNA (but not AT1R/AT2R protein) and impaired recovery. Other groups (except CHA) did not improve recovery. The results suggest that, in isolated working hearts, AT2R plays a significant role in ischemia-reperfusion and AT2R blockade induces increased AT2R protein and cardioprotection.

angiotensin II; angiotensin II type 1 receptor; angiotensin II type 2 receptor


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