An intracardiac production of aldosterone has been recently reported in rat. Angiotensin II results in increased inotropy, chronotropy, catecholamine (norepinephrine) release, catecholamine sensitivity, aldosterone levels, vasopressin levels, and cardiac remodeling and vasoconstriction through AT1 receptors on peripheral vessels (conversely, AT2 receptors impair cardiac remodeling). Cardiac aldosterone production and ventricular remodeling. SA and PA patients showed markedly elevated aldosterone levels (67 versus 39 ng/dL, respectively; normal values <15 ng/dL) but contrasting values of plasma renin activity (15.00 versus 0.56 ng/mL/h; P<0.001). Therefore, aldosterone receptor blockade is cardiac protective in chronic CHF and may be important in the acute remodeling events after MI. Cardiac remodeling is a deleterious consequence of arterial hypertension. Excessive activation of the neuroendocrine system can promote ventricular remodeling after acute myocardial infarction (AMI). … cardiac or ventricular remodeling) in response to hemodynamic load and/or cardiac injury, in association with neurohormonal activation and other factors.The process of cardiac remodeling includes structural… This topic will discuss the hemodynamic and remodeling aspects of … Listing a study does not mean it has been evaluated by the U.S. Federal Government. Heart failure is one of the major public health challenges facing the Western world. Considering that aldosterone affects cardiovascular remodeling in pathological states, it may play a role in regulating fetal cardiac development. Thus, an aldosterone-induced expression of TNX in cardiomyocytes could lead to disturbed collagen deposition and extracellular matrix remodeling as well as cardiac fibrosis, which have been demonstrated to occur after prolonged mineralocorticoid and high salt treatment . An intracardiac production of aldosterone has been recently reported in rat. Cardiac remodeling is generally accepted as a determinant of the clinical course of heart failure (HF). The proinflammatory and profibrotic effects of the RAAS are also mediated by aldosterone. Rationale 1: The cardiac remodeling from angiotensin II does not cause hypotrophy of myocyte cells, but rather hypertrophy of myocyte cells. This production is increased both acutely and chronically by angiotensin II, observations suggesting that the heart contains a steroidogenic system that is regulated similarly to the adrenal one. Angiotensin II and aldosterone often collaborate in pathological situations to induce hypertrophy of cardiomyocytes, vascular inflammation, perivascular and interstitial fibrosis, and microvascular rarefaction. An intracardiac production of aldosterone has been recently reported in rat. Another important pillar in the vascular remodeling process is the RAAS [40, 41]. Relation Between Aldosterone and Cardiac Remodeling After Myocardial Infarction (REMI) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. To evaluate its participation, we studied the expression of AT1R and AT2R at the vascular level. Abstract: DESCRIPTION (provided by applicant): Aldosterone is implicated in the process of myocardial remodeling and failure .