%0 Journal Article
%T The Relationship between Reactive Oxygen Species and Cardiac Fibrosis in the Dahl Salt-Sensitive Rat under ACEI Administration
%A Ryou Tanaka
%A Miki Shimizu
%J Veterinary Medicine International
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/105316
%X Enalapril maleate, the oldest and most widely distributed ACEI, and alacepril, the newest and antioxidant ACEI, were compared in the point of cardioprotective effect for Dahl salt-sensitive rat. In order to evaluate the correlation between the three factors, cardiac fibrosis and blood pressure/oxidative-stress marker (tissue TBARS), index of correlation was calculated. The results showed a significant difference in cardiac fibrosis between high-dose alacepril (30£¿mg/kg/day, group H) and enalapril maleate (10£¿mg/kg/day, group E). There was significant correlation between cardiac fibrosis and oxidative-stress marker, although there was no correlation between cardiac fibrosis and blood pressure. Fibrosis was more influenced by oxidative stress not by blood pressure, we should not select ACEI only by blood pressure-lowering effect and should more consider cardioprotective effects of ACEI. 1. Introduction Heart failure is defined as a syndrome that demonstrates a systolic dysfunction, diastolic dysfunction, or both. There are many mechanisms by which heart failure can be induced. However, cardiac remodeling and sequential fibrosis of cardiac muscle seems to contribute equally to cardiac failure. Although many factors are referred to as causative agents in cardiac remodeling, the renin-angiotensin system (RAS), sympathetic nerve system, and reactive oxygen species (ROS) are considered the major factors that intricately interact with each another. Because angiotensin II (Ang II) is generated by the RAS and induces the activation of sympathetic nerve system and augmentation of ROS, regulation of the RAS is recognized as an important measure for preventing fibrosis of cardiac muscle. Two types of RAS, circulating RAS and cardiac RAS, which act in different ways have been reported [1¨C6]. Circulating RAS is activated in response to decreased cardiac output where it increases blood pressure by constricting the peripheral vessels mainly via sodium retention. Cardiac RAS directly stimulates cardiomyocyte hypertrophy and fibroblast proliferation, which leads to left ventricular hypertrophy, diastolic and systolic dysfunction, arrhythmia, heart failure, and, ultimately, cardiac cell death. To maintain the cardiac function, inhibition of cardiac RAS seems important, and many types of angiotensin-converting enzyme inhibitors (ACEIs) are used for this purpose [7]. Various types of ACEIs with very similar basic vasodepressive effects are available; however, they differ slightly in their pharmacokinetics. To stabilize the therapeutic effect and minimize the adverse effects,
%U http://www.hindawi.com/journals/vmi/2012/105316/