Abstract
All the components of the kallikrein-kinin system are located in the cardiac muscle andits deficiency may lead to cardiac dysfunction. In recent years, numerous observationsobtained from clinical and experimental models of diabetes, hypertension, cardiacfailure, ischemia, myocardial infarction, and left ventricular hypertrophy have suggestedthat the reduced activity of the local kallikrein-kinin system may be instrumental for theinduction of cardiovascular-related diseases. The cardioprotective property of theangiotensin-converting enzyme inhibitors is primarily mediated via a kinin-releasingpathway, which may cause regression of the left ventricular hypertrophy in hypertensivesituations. The ability of kallikrein gene delivery to produce a wide spectrum of beneficialeffects makes it a promising candidate in treating hypertension and cardiovascular andrenal diseases. In addition, stable kinin agonists may also be available in the future astherapeutic agents for cardiovascular and renal disorders. However, there are alsopossibilities of adverse effects that may be caused by these compounds.
Highlights
A number of observations focus on the kinins as potential mediators in endogenous, cardiovascular protective mechanisms
BK at a dose that has no effect on blood pressure (BP) can prevent left ventricular hypertrophy (LVH) in rats with hypertension caused by aortic banding[11]
We have demonstrated for the first time that a lack of the cardiac kallikrein-kinin system (KKS) could be responsible for the induction of LVH in spontaneously hypertensive rats (SHR) and SHR with diabetes[2,3,4]
Summary
All the components of the kallikrein-kinin system are located in the cardiac muscle and its deficiency may lead to cardiac dysfunction. Numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction, and left ventricular hypertrophy have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular-related diseases. The cardioprotective property of the angiotensin-converting enzyme inhibitors is primarily mediated via a kinin-releasing pathway, which may cause regression of the left ventricular hypertrophy in hypertensive situations. The ability of kallikrein gene delivery to produce a wide spectrum of beneficial effects makes it a promising candidate in treating hypertension and cardiovascular and renal diseases. Stable kinin agonists may be available in the future as therapeutic agents for cardiovascular and renal disorders.
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