Aldosterone is a mineralocorticoid secreted by the zona glomerulosa of the adrenal cortex in response to decreased serum sodium, decreased blood volume, and increased serum potassium. When needed, aldosterone also acts to increase sodium reabsorption in the renal tubules, resulting in potassium excretion and increased water retention, blood volume, and blood pressure. Changes in renal blood flow trigger or suppress release of renin from the glomeruli. The presence of circulating renin stimulates the liver to produce angiotensin I. Angiotensin I is converted by the lung and kidney into angiotensin II, a potent trigger for the release of aldosterone. Aldosterone and the renin-angiotensin system work together to regulate sodium and potassium levels. This test is of little diagnostic value in differentiating primary and secondary aldosteronism unless plasma renin activity is measured simultaneously (see monograph titled “Renin”). A variety of factors influence serum aldosterone levels, including sodium intake, certain medications, and activity. Secretion of aldosterone is also affected by ACTH, a pituitary hormone that primarily stimulates secretion of glucocorticoids and minimally affects secretion of mineralocorticosteroids. Patients with serum potassium less than 3.6 mEq/L and 24-hour urine potassium greater than 40 mEq/L fit the general criteria to test for aldosteronism. Renin is low in primary aldosteronism and high in secondary aldosteronism. A ratio of plasma aldosterone to plasma renin activity greater than 50 is significant. Ratios greater than 20 obtained after unchallenged screening may indicate the need for further evaluation with a sodium-loading protocol. A captopril protocol can be substituted for patients who may not tolerate the sodium-loading protocol.