Abstract

Bradykinin is a peptide consisting of nine amino acids, which is generated by the plasma kallikrein-kinin system as well as the glandular (tissue) kallikrein-kinin system and plasma aminopeptidase (Fig. 11-1). There are at least two classes of bradykinin receptors, i.e. Bl and B2 receptors, and bradykinin exerts its action on most of the cardiovascular system through B2 receptors. Although bradykinin production in ischemic myocardium was first reported almost 30 years ago, the significance of kinin in myocardial ischemic injury did not receive wide-spread attention for decades. Recently, a specific and potent B2 receptor antagonist Hoe 140 (icatibant) became available, and several important aspects of bradykinin in the pathophysiology of myocardial ischemia have been clarified in the past several years. Firstly, it has been suggested that activation of the B2 receptor before ischemia may protect the heart against ischemia/reperfusion injury, including arrhythmia, contractile dysfunction and necrosis. Secondly, bradykinin may play a role in an endogenous cardioprotective mechanism, ischemic preconditioning (i.e. cardioprotective effect of brief transient non-lethal ischemia). This article briefly reviews the involvement of bradykinin in the enhancement of myocardial tolerance against infarction by ischemic preconditioning.

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