The renin-angiotensin-aldosterone system (RAAS) is the primary hormonal regulator of blood pressure, fluid volume, and electrolyte balance, operating through a cascade involving the kidneys, liver, lungs, and adrenal glands. The cascade initiates at the juxtaglomerular (JG) apparatus, located where the distal convoluted tubule (macula densa) contacts the afferent arteriole of its own glomerulus. Three stimuli trigger renin release from JG cells: (1) decreased renal perfusion pressure sensed by baroreceptors in the afferent arteriole, (2) decreased NaCl delivery to the macula densa (sensed via the Na-K-2Cl cotransporter), and (3) increased sympathetic nervous system activation via beta-1 adrenergic receptors on JG cells. Renin cleaves angiotensinogen (constitutively produced by the liver) to angiotensin I (inactive). Angiotensin-converting enzyme (ACE), concentrated in pulmonary capillary endothelium, converts angiotensin I to angiotensin II — the primary effector. Angiotensin II exerts its effects through AT1 receptors: arteriolar vasoconstriction (especially efferent arteriolar constriction maintaining GFR), stimulation of aldosterone secretion from the zona glomerulosa of the adrenal cortex, stimulation of ADH release from the posterior pituitary, enhancement of proximal tubular sodium reabsorption, stimulation of thirst via circumventricular organs, and promotion...