Aldosterone antagonists reduce mortality in chronic heart failure (CHF). An obvious question to ask is how do they do this. The prevailing hypothesis is that most of the adverse effects of aldosterone stem from its ability to produce a vasculopathy. This vasculopathy is characterised by a reduction in vascular nitric oxide and may be produced by aldosterone's ability to generate superoxide radicals which degrade endogenous NO. The consequences of this "aldosterone-induced vasculopathy" are that it produces tissue ischaemia/infarction and injury, which then repairs itself by producing fibrosis. "Aldosterone-induced vasculopathy" may be the main mechanism why aldosterone promotes widespread tissue injury and ultimately cardiac death.
|Number of pages||3|
|Journal||Molecular and Cellular Endocrinology|
|Publication status||Published - 2004|
|Event||International symposium on aldosterone - London, United Kingdom|
Duration: 28 Apr 2003 → 30 Apr 2003