• 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. Hormonal • 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 pressure • 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