Cardioprotective Effects of Angiotensin Converting Enzyme II

Abstract

To circumvent the major threats of low blood volume and low blood pressure, animals need powerful mechanisms for salt and water conservation, which is renin–angiotensin system (RAS). Activation of RAS is therefore a useful response in many demanding situations. However, an increased activity of the RAS, especially in combination with other cardiovascular risk factors, may lead to a cascade of deleterious effects such as hypertension, atherosclerosis, myocardial remodeling, heart failure, ischemic stroke, and diabetes mellitus. Many of these pathophysiological actions of angiotensin II (Ang II) may still be viewed as being homeostatic in principle but harmful if carried to excess. Numerous experimental studies have indicated that angiotensin‑converting enzyme II (ACE II) efficiently hydrolyzes the potent vasoconstrictor Ang II to Ang 1–7. Thus, the axis formed by ACE II/Ang 1–7/Mas appears to represent an endogenous counter‑regulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/proliferative arm of the RAS consisting of ACE, Ang II, and Ang II Type 1 receptor (AT1R). Although most of the well‑known cardiovascular and renal effects of RAS are attributed to ACE, an important enzyme in the generation of Ang II, much less is known about the functions of ACE II. This review summarizes recently published data on the basic properties of ACE II and Ang 1–7 and a summary of the evidence from experimental and clinical studies of various pathological conditions related to the biological roles of ACE II/Ang 1–7/Mas in the heart.