Role of kinins in myocardial ischemia

TL;DRAbstract

Kinins are potent vasoactive and inflammatory peptides derived from plasma precursors under conditions of tissue injury and ischemia [1]. Their vasoactive effects are mainly mediated through the release of different autacoids, generated by the endothelium. Recent evidence has been accumulated that the endothelium itself can release kinins [2]. Activation of G protein coupled endothelial B2 kinin receptors, leads (by stimulating phospholipases C and A2) to the formation of the potent vasodilators nitric oxide (NO) and prostacyclin (PGI2) [2]. In blood vessels kininase II or angiotensin converting enzyme (ACE) is located mainly at the luminal surface of the endothelial cell membrane and appears to be largely responsible for the local proteolytic breakdown of vascular kinins [3]. Thus under physiological conditions the effect of vascular generated and released kinins is limited by the activities of endothelial ACE and enzymes in deeper layers of the vascular wall [4]. However, if the brea

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