The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and sodium levels through a hormonal cascade. Renin is released by the kidneys in response to low blood pressure, volume, or sodium and converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme then converts angiotensin I to angiotensin II, which causes vasoconstriction, sodium retention, and aldosterone release. This increases blood pressure and volume. ACE inhibitors and angiotensin receptor blockers are used to treat hypertension by inhibiting this system.
The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and sodium levels through a hormonal cascade. Renin is released by the kidneys in response to low blood pressure, volume, or sodium and converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme then converts angiotensin I to angiotensin II, which causes vasoconstriction, sodium retention, and aldosterone release. This increases blood pressure and volume. ACE inhibitors and angiotensin receptor blockers are used to treat hypertension by inhibiting this system.
The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and sodium levels through a hormonal cascade. Renin is released by the kidneys in response to low blood pressure, volume, or sodium and converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme then converts angiotensin I to angiotensin II, which causes vasoconstriction, sodium retention, and aldosterone release. This increases blood pressure and volume. ACE inhibitors and angiotensin receptor blockers are used to treat hypertension by inhibiting this system.
• 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