The renin-angiotensin-aldosterone system (RAAS) is a major regulator of blood pressure control, fluid, and electrolyte balance in humans. Chronic activation of
mineralocorticoid production leads to dysregulation of the cardiovascular system and to
hypertension. The key
mineralocorticoid is
aldosterone.
Hyperaldosteronism causes
sodium and fluid retention in the kidney. Combined with the actions of
angiotensin II, chronic elevation in
aldosterone leads to detrimental effects in the vasculature, heart, and brain. The adverse effects of excess
aldosterone are heavily dependent on increased dietary
salt intake as has been demonstrated in animal models and in humans.
Hypertension develops due to complex genetic influences combined with environmental factors. In the last two decades, primary
aldosteronism has been found to occur in 5% to 13% of subjects with
hypertension. In addition, patients with
hyperaldosteronism have more end organ manifestations such as
left ventricular hypertrophy and have significant cardiovascular complications including higher rates of
heart failure and
atrial fibrillation compared to similarly matched patients with
essential hypertension. The pathophysiology, diagnosis, and treatment of primary
aldosteronism will be extensively reviewed. There are many pitfalls in the diagnosis and confirmation of the disorder that will be discussed. Other rare forms of hyper- and hypo-
aldosteronism and unusual disorders of
hypertension will also be reviewed in this article.