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Updated: Oct 17 2021

Renin-Angiotensin-Aldosterone System

  • Overview
  • Introduction
    • The renin-angiotensin-aldosterone system (RAAS) attempts to maintain arterial blood pressure by controlling blood volume
      • a decrease in arterial blood pressure is sensed by the kidneys as decreased renal perfusion pressure
        • this in turn stimulates the juxtaglomerular cells to secrete renin into circulation
          • note that increased sympathetic activity and β1-agonists (e.g., isoproterenol) increase renin secretion
          • renin converts angiotensinogen into angiotensin I, a precursor of angiotensin II
            • angiotensin-converting enzyme (ACE) in the lung and kidneys converts angiotensin I → angiotensin II
        • note that a decrease in Na+ delivery to the macula densa also stimulates RAAS
      • angiotensin II activates type I G protein-coupled angiotensin II receptors (AT1) receptors which
        • acts on the adrenal cortex (zona glomerulosa) to increase aldosterone secretion
          • aldosterone will increase Na+ reabsorption and K+ secretion in the principal cells of the distal tubule and collecting duct
          • aldosterone will also increase H+ secretion in the alpha-intercalated cells
        • directly stimulates the Na+-H+ exchange
        • acts on the hypothalamus to increase thirst and the pituitary to increase anti-diuretic hormone (ADH) secretion
          • ADH will act on the principal cells to increase aquaporin-2 expression
            • this increases the collecting duct's permeability to water and thus increases water reabsorption
        • acts on arterioles to increase total peripheral resistance and thus increasing arterial pressure
        • preferrentially constricts the efferent arteriole to maintain glomerular filtration rate (GFR) in low volume states (e.g., hemorrhaging)
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