New perspective on the tissue kallikrein-kinin system in myocardial infarction: role of angiogenesis and cardiac regeneration.

An intensification of the local cardiac kallikrein-kinin system (KKS) is thought to delay the development of cardiac failure. Since myocardial infarction is one of the leading causes of death in the developed countries, the role of the kallikrein-kinin system was studied in numerous experimental studies focusing on this disease using strategies like kallikrein gene transfer, tissue kallikrein infusion and/or by use of human kallikrein over expressing animals. These studies suggested that the kallikrein-kinin system increases coronary blood flow, decreases infarct size and left ventricular remodeling post myocardial infarction. This is of special interest since pharmacological inhibition of the angiotensin converting enzyme acts not only by reducing angiotensin II levels, but also by preventing enzymatic breakdown of kinins, suggesting that the kallikrein-kinin system is part of ACE inhibition effects. Here we review the current concept of the kallikrein-kinin system during myocardial infarction with special regard to its effects on angiogenesis and myocardial regeneration.