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Published on: June 7, 2016
Review of aldosterone- and angiotensin II-induced target organ damage and prevention
Allan D Struthers1, Thomas M MacDonald
1Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Tayside DD1 9SY, Dundee, UK. a.d.struthers@dundee.ac.uk
Abstract:
Aldosterone is well recognized as a cause of sodium reabsorption, water retention, and potassium and magnesium loss; however, it also produces a variety of other actions that lead to progressive target organ damage in the heart, vasculature, and kidneys. Aldosterone interacts with mineralocorticoid receptors to promote endothelial dysfunction, facilitate thrombosis, reduce vascular compliance, impair baroreceptor function, and cause myocardial and vascular fibrosis. Although angiotensin II has been considered the major mediator of cardiovascular damage, increasing evidence suggests that aldosterone may mediate and exacerbate the damaging effects of angiotensin II. While angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers reduce plasma aldosterone levels initially, aldosterone rebound, or 'escape' may occur during long-term therapy. Therefore, aldosterone blockade is required to reduce the risk of progressive target organ damage in patients with hypertension and heart failure. This may be achieved nonselectively with spironolactone or with use of the selective aldosterone blocker eplerenone. While both agents have been demonstrated to be effective antihypertensive agents, eplerenone may produce improved target organ protection as witnessed in a variety of clinical settings, without the antiandrogenic and progestational effects commonly observed with spironolactone.
Insights
Aldosterone blockade is crucial for preventing organ damage in hypertension and heart failure. Selective aldosterone blockers like eplerenone offer improved protection over non-selective agents without side effects.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Nephrology
Background:
- Aldosterone causes sodium retention and potassium loss, contributing to target organ damage.
- It exacerbates cardiovascular and renal damage, potentially mediating angiotensin II's effects.
- Aldosterone 'escape' can occur with ACE inhibitors and ARBs, necessitating blockade.
Purpose of the Study:
- To highlight aldosterone's role in target organ damage beyond sodium reabsorption.
- To emphasize the need for aldosterone blockade in managing hypertension and heart failure.
- To compare the efficacy and side effect profiles of selective and non-selective aldosterone blockers.
Main Methods:
- Review of existing literature on aldosterone's effects and blockade therapies.
- Analysis of clinical evidence for aldosterone antagonists in cardiovascular and renal protection.
- Comparison of spironolactone and eplerenone in terms of efficacy and tolerability.
Main Results:
- Aldosterone blockade is essential for mitigating progressive target organ damage.
- Eplerenone demonstrates improved target organ protection compared to spironolactone.
- Eplerenone offers benefits without the antiandrogenic and progestational side effects of spironolactone.
Conclusions:
- Aldosterone blockade is a vital therapeutic strategy for patients with hypertension and heart failure.
- Selective aldosterone blockade with eplerenone provides superior organ protection.
- Eplerenone represents an effective and well-tolerated option for aldosterone antagonism.
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01:29Hypertension II: Pathophysiology
01:29Heart Failure II: Pathophysiology