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)