The hormone aldosterone is produced from cholesterol in the adrenal cortex. It is a mineralocorticoid and binds to mineralocorticoid receptors in the kidneys, heart, blood vessels, liver and in other tissues. Aldosterone is regulated via the renin-angiotensin-aldosterone system (RAAS). It acts mainly in the kidneys, increasing the resorption of sodium from the distal tubules and the excretion of potassium. An increase in the potassium level increases the blood volume and blood pressure.
Hyperaldosteronism may be primary or secondary. The most frequent symptom is hypertension, accompanied by fatigue, headache, polyuria and polydipsia. Up to 10 % of all hypertonia cases are caused by primary hyperaldosteronism. The secondary form is less frequent.
Primary hyperaldosteronism (Conn's syndrome) is caused by overproduction of aldosterone in the adrenal cortex. In two thirds of cases the aetiology is idiopathic bilateral adrenal hyperplasia and in one third it is an underlying tumour in the zona glomerulosa. In primary hyperaldosteronism, the renin level is also low. It may be completely suppressed in manifest disease. Secondary hyperaldosteronism is a consequence of overstimulation of the RAAS. In secondary hyperaldosteronism, the aldosterone and renin levels are increased. In suspected cases of hyperaldosteronism, the ratio of aldosterone to renin in plasma should be determined.
The aldosterone level is low in chronic adrenal cortex insufficiency (Addison’s disease) and anterior hypopituitarism.
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