ABSTRACT
The concept that the renin–angiotensin–aldosterone system (RAAS) plays a major role in determining cardiovascular (CV) structure and function, in both health and disease, is now firmly ensconced in the thinking of clinicians and researchers alike. Widespread recognition of its importance, new information about how the RAAS is regulated, the signaling pathways through which it alters cell functions and the ways in which it affects the CV system continue to emerge. The initial description of the RAAS depicted a cascade of events that occurred mainly within the blood stream and which culminated in the production of Ang II. Cardiac remodeling has been defined as “genome expression, molecular, cellular and interstitial changes that are manifested clinically as changes in size, shape and function of the heart after cardiac injury”. In the post-myocardial infarction heart, there is evidence of cardiac myocyte hypertrophy and lengthening, ongoing myocyte loss due to apoptosis, and restructuring of the extracellular matrix.
