The renin-angiotensin-aldosterone system (RAAS) is a critical regulator of blood pressure and fluid balance. When blood pressure drops, the juxtaglomerular cells of the afferent arteriole release renin; the three triggers are reduced stretch of the afferent arteriole, reduced sodium chloride delivery to the macula densa, and beta-1 sympathetic stimulation. Renin is an enzyme that catalyzes the conversion of angiotensinogen (made by the liver) into angiotensin I. Angiotensin I is then converted into angiotensin II by angiotensin-converting enzyme (ACE), found mainly on the pulmonary endothelium. Angiotensin II acts as a potent vasoconstrictor, increasing systemic blood pressure by narrowing blood vessels. It also stimulates the release of aldosterone from the adrenal glands, which promotes sodium and water retention in the kidneys, further increasing blood pressure. Additionally, angiotensin II stimulates the release of ADH, which enhances water reabsorption in the kidneys, contributing to blood pressure regulation. Within the kidney itself, angiotensin II constricts the efferent arteriole more than the afferent, which keeps glomerular capillary pressure and GFR up when renal perfusion falls. This is the mechanism behind two perioperative cautions. Patients taking an ACE inhibitor or an angiotensin receptor blocker lose that efferent support, so hypotension under anesthesia translates more directly into a fall in GFR, and these drugs are associated with more intraoperative hypotension, which can be resistant to ephedrine and phenylephrine (vasopressin is the usual rescue); whether to hold them on the morning of surgery is decided case by case, and many practices hold them when taken for hypertension alone and continue them for heart failure. Nonsteroidal anti-inflammatory drugs act on the other arteriole: prostaglandins dilate the afferent arteriole during stress and hypovolemia, and an NSAID removes that protection.
Through the RAAS, the kidneys exert control over blood volume, electrolyte balance, and systemic vascular resistance, which are vital for maintaining homeostasis in the face of changing physiological demands.
| Hormone or mediator | Origin or trigger | Action |
|---|---|---|
| Erythropoietin | Produced by the kidney in response to low oxygen levels in the blood | Stimulates red blood cell production |
| Renin | Released by the kidney when blood pressure drops | Catalyzes conversion of angiotensinogen into angiotensin I, opening the RAAS cascade |
| Angiotensin II | Converted from angiotensin I by angiotensin-converting enzyme | Potent vasoconstrictor that raises systemic blood pressure; also stimulates release of aldosterone and ADH |
| Aldosterone | Released from the adrenal glands under angiotensin II stimulation | Promotes sodium and water retention, increasing sodium reabsorption in the distal tubule and collecting ducts by promoting sodium channel synthesis; also regulates potassium secretion |
| Antidiuretic hormone | Released under angiotensin II stimulation | Increases the number of aquaporins in the collecting duct membrane, enhancing water reabsorption |
| Calcitriol | The kidney converts vitamin D into this active form | Essential for calcium homeostasis and bone health |
| Parathyroid hormone | Released by the parathyroid glands when ionized calcium falls | Regulates calcium uptake in the distal convoluted tubule and collecting ducts |
