Adaptive and genetic alterations of the renin angiotensin system in cardiac hypertrophy and failure
Abstract
The risk to suffer from cardiovascular events may be modulated, in part, by neurohormonal systems. Neurohormones such as angiotensin II or aldosterone may be activated secondary to congestive heart failure or in the course of an acute myocardial infarction. These systems, if activated, will subject the failing heart to increased hemodynamic load and, thus, further compromise cardiac function. In addition, structural changes of the heart and vessels occurring with pressure or volume overload may be amplified by the growth promoting effects of these agents. Taken together, the interaction of underlying cardiovascular disease and activated neurohormones may often determine clinical symptoms and prognosis. More recently, growing evidence suggests that the basal, genetically determined, activity of the renin angiotensin aldosterone system may relate to the development of cardiovascular disease as well. In particular, variants of the angiotensinogen and angiotensin converting enzyme genes have been associated with essential hypertension, myocardial infarction, or left ventricular hypertrophy. In this regard, the data suggest that the renin angiotensin aldosterone system may be one of the primary causes, rather than only a secondary c...Continue Reading
References
Changes in cardiac angiotensin converting enzyme after myocardial infarction and hypertrophy in rats
Citations
ACE-DD genotype is associated with the occurrence of acute coronary syndrome in postmenopausal women
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