Hepatic modulation of kinin system in experimental diabetes model

Abstract

Kinins are peptides formed by 8-11 amino acids, such as bradykinin, kallidin and their metabolites. It has biological action by binding to membrane receptors B1 and B2. It has indirect vasodilating action, by stimulating the production of nitric oxide and are related to inflammatory conditions. In the arterial system bradykinin has hypotensive effect, while in the portal system has hypertensive action mediated by B2 receptors (via nitric oxide). It was found experimentally that during the process of liver cirrhosis and partial hepatoctemy there is increased expression of B1 receptor, suggesting a role of this receptor in fibrogenesis and cellular remodeling that occurs in these situations. In pathological processes such as diabetes, there was an increase in B1 receptor signaling pathway in certain tissues, mainly central nervous system, suggesting that hyperglycemia is a stimulus for the kallikrein-kinin system.Thus, this project aims to study the expression or absence of kinin receptors in the liver of animals undergoing experimental model of diabetes and verify their possible role in carbohydrate metabolism (glycolysis and gluconeogenesis).