期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 282, 期 4, 页码 H1206-H1215出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00839.2000
关键词
angiotensin II; angiotensin II type 1 receptor; angiotensin II type 2 receptor
We assessed ANG II type 1 (AT(1)) and type 2 (AT(2)) receptor (R) expression and functional recovery after ischemia-reperfusion with or without AT(1)R/AT(2)R 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 AT(1)R antagonist; 1 mumol/l), PD-123319 (an AT(2)R antagonist; 0.3 mumol/l), N-6-cyclohexyladenosine (CHA, a cardioprotective adenosine A(1) receptor agonist; 0.5 mumol/ l as positive control), enalaprilat (an ANG-converting enzyme inhibitor; 1 mumol/l), PD-123319 + losartan, ANG II (1 nmol/ l), or ANG II + losartan. Compared with controls, ischemia-reperfusion decreased AT(2)R protein (Western immunoblots) and mRNA (Northern immunoblots, RT-PCR) and impaired functional recovery. PD-123319 increased AT(2)R protein and mRNA and improved functional recovery. Losartan increased AT(1)R mRNA (but not AT(1)R/AT(2)R protein) and impaired recovery. Other groups (except CHA) did not improve recovery. The results suggest that, in isolated working hearts, AT(2)R plays a significant role in ischemia-reperfusion and AT(2)R blockade induces increased AT(2)R protein and cardioprotection.
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