1, 3 4- 5 Without intervention, a failing heart will become victim of the body’s own compensatory mechanisms in an uncontrolled downward spiral of further hormonal activation, fluid retention, tissue remodeling and pump failure. With the increase in circulating volume, which may promote systemic congestion, aldosterone directly promotes myocyte hypertrophy, fibrosis, atherosclerosis, reduced baroreceptor sensitivity, and decreased nitric oxide availability among other deleterious effects. In heart failure, this cascade of actions is more detrimental than supportive as hypoperfusion is primarily related to a decreased cardiac output, secondary to decreased pump function not hypotension. Even though there is now evidence of local production of aldosterone by failing cardiac tissues, aldosterone production is primarily dependent upon the activation of systemic RAAS. ![]() 1 Each year our knowledge base becomes more nuanced, and the complex roles of each hormone become further elucidated. ![]() Cardiac remodeling and the progression of heart failure driven by the renin-angiotensin-aldosterone system (RAAS) has been an area of interest for over five decades.
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