Pathophysiology
Clinical meaning
The renin-angiotensin-aldosterone system (RAAS) is the primary hormonal regulator of blood pressure, sodium balance, and potassium homeostasis. Decreased renal perfusion pressure or sympathetic stimulation triggers juxtaglomerular cells to release renin, which cleaves angiotensinogen (from the liver) to angiotensin I. Angiotensin-converting enzyme (ACE) in pulmonary endothelium converts angiotensin I to angiotensin II, which causes potent arteriolar vasoconstriction, stimulates aldosterone secretion from the zona glomerulosa, promotes ADH release, and stimulates thirst. Aldosterone acts on the distal convoluted tubule and collecting duct via mineralocorticoid receptors, upregulating epithelial sodium channels (ENaC) and Na+/K+-ATPase, increasing sodium and water reabsorption while excreting potassium and hydrogen ions. Primary aldosteronism (Conn syndrome) involves autonomous aldosterone production (usually from adrenal adenoma or bilateral hyperplasia), causing sodium retention, hypertension, hypokalemia, and metabolic alkalosis. It is the most common cause of secondary hypertension, affecting 5-13% of hypertensive patients.