Hyperaldosteronism may be primary or secondary. Most cases of primary hyperaldosteronism are due to benign
aldosterone-producing adrenal adenomas. The remainder are due to bilateral adrenal hyperplasia. Rarely, adrenal carcinoma can cause primary hyperaldosteronism. The incidence is three times higher in women than in men and is highest between ages 30 and 50.

In primary hyperaldosteronism, chronic aldosterone excess is independent of the renin-angiotensin-aldosterone system and in fact suppresses plasma renin activity. This aldosterone excess enhances sodium reabsorption by the kidneys, which leads to mild hypernatremia and, simultaneously, hypokalemia and increased extracellular fluid volume. Expansion of intravascular fluid volume also occurs and results in volume-dependent hypertension and increased cardiac output.

Excessive ingestion of English black licorice or licorice-like substances can produce a syndrome similar to primary hyperaldosteronism due to the mineralocorticoid action of glycyrrhizic acid.

Secondary hyperaldosteronism results from an extra-adrenal abnormality that stimulates the adrenal gland to increase production of aldosterone. For example, conditions that reduce renal blood flow (renal artery stenosis) and extracellular fluid volume or produce a sodium deficit activate the renin-angiotensin-aldosterone system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms’ tumor), ingestion of hormonal contraceptives, and pregnancy.