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Renin-angiotensin-aldosterone system (RAAS)

• Description: hormonal system that regulates arterial blood pressure and

sodium concentration
• Mechanism: renal hypoperfusion (e.g., hypotension, hypovolemia),
hyponatremia or increased sympathetic tone → kidneys release renin
(produced in the juxtaglomerular apparatus) → renin converts
angiotensinogen (produced in the liver) to angiotensin I → conversion of
angiotensin I to angiotensin II through angiotensin-converting enzyme
(ACE, mostly produced in the lungs) → Angiotensin II acts as a strong
vasoconstrictor and induces the secretion of aldosterone by the adrenal
cortex → aldosterone increases renal reabsorption of sodium (and water)
and augments the excretion of potassium and protons → ↑ extracellular
fluid, ↑ blood pressure, ↓ K+, ↑ pH
• Effects
• Systemic: ↑ arterial blood pressure
• Renal: maintains GFR during renal hypoperfusion

ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II.

Angiotensin receptor blockers inhibit the effect of angiotensin II. Both drug
classes are used to treat arterial hypertension.
• Natriuretic peptides
• Atrial natriuretic peptide (ANP): volume overload → dilation of atria →
secretion of ANP by myocytes
• Brain natriuretic peptide (BNP): volume overload → dilation of ventricles
→ secretion of ANP by myocytes
• Inhibits epithelial Na2+ transporter in the collecting duct →
increased water secretion → lowering the central venous
• Inhibits secretion of aldosterone, renin, ADH, and ACTH
• Antidiuretic hormone (ADH)
• Increases contraction of smooth muscle in blood vessels via V1 receptor
→ increased blood pressure → increased kidney perfusion
• Increases free water reabsorption in the collecting duct (stimulation of
adenylate cyclase → ↑ cAMP → incorporation of aquaporins in the
luminal membrane of collecting ducts)
• Increases urea resorption (↑ incorporation of urea transporters in the
collecting duct)
Autonomic regulation
• Mechanism
• Noradrenaline → binds to α1 receptors → vasoconstriction of arterioles
→ ↑ resistance → ↓ renal blood flow
• Dopamine → binds to D1 receptors → vasodilatation of arterioles → ↓
resistance → ↑ renal blood flow
Hypovolemic shock with severe hypotension activates the sympathetic nervous
system. Subsequently, the hypovolemia and noradrenaline-induced
vasoconstriction result in low renal blood flow → low GFR → low urine production
→ acute renal injury