Effect of des-aspartate-angiotensin I on myocardial ischemia-reperfusion injury in rats and on release of prostanoids by human umbilical vein endothelial cells
WEN QIANG
WEN QIANG
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Abstract
The effect of des-aspartate-angiotensin I (DAA-I) on myocardial ischemia-reperfusion injury was studied. In rats subjected to myocardial ischemia-reperfusion injury, DAA-I was effective in reducing infarct size, lowering serum creatine kinase, decreasing tissue myeloperoxidase and inhibiting the expression of ICAM-1. The cardioprotective effects of DAA-I could be blocked by indomethacin. Investigational efforts were also directed to the prostanoid release in response to DAA-I in human umbilical vein endothelial cells (HUVEC). DAA-I at lower concentration, i.e. 10-10 M, stimulated the release of PGE2 and PGI2, but not PGF2I? and TXA2, through the AT1 receptor and COX-1 in HUVEC. While DAA-I at higher concentration, i.e. 10-5 M, stimulated the release of not only PGE2 and PGI2, but also PGF2I? through the AT1 receptor and COX-2. It is possible that DAA-I at different concentration binds to different functional form of the AT1 receptor to stimulate different profile of prostanoids.
Keywords
des-aspartate-angiotensin I, AT1 receptor, myocardial ischemia, reperfusion, ICAM-1, prostanoid
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2004-11-04
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