Aldosterone is a salt corticosteroid synthesized and secreted by the adrenal cortex in the globus pallidus, which acts on the distal tubules and collecting ducts of the kidney, exerting sodium- and potassium-retaining and hydrogen-secreting effects. The secretion of aldosterone is mainly regulated by the RAS, and ACTH plays a very important role in regulating aldosterone, although it is not as clear as that of cortisol. In addition, aldosterone secretion is also regulated by potassium. Clinical significance: Normal aldosterone levels need to be assessed in conjunction with blood and urine electrolytes. In normal subjects, urinary potassium excretion is a reliable indicator of potassium homeostasis, but not in patients with hyperaldosteronism, who lose large amounts of potassium from the urine daily due to the potassium excretion of aldosterone, even though potassium intake and blood potassium levels are already very low. Clinically, when blood potassium is <3.5 mmol > 40 mmol/L, this indicates excessive urinary potassium excretion and is strong evidence in favor of aldosteronism. At this point, a combination of PRA is needed to identify whether the aldosteronism is primary or secondary. 1, increased blood and urine aldosterone: seen in primary aldosteronism, secondary aldosteronism (such as renal artery stenosis, congestive heart failure, cirrhotic ascites or nephrotic syndrome), female luteal phase, pregnancy and the application of certain drugs such as diuretics, birth control pills and estrogen. 2, blood urinary aldosterone decreased: seen in congenital adrenal cortical hyperplasia (17a- and 11β-hydroxylase deficiency), Liddle syndrome, Addison’s disease and the application of certain drugs such as beta-blockers.