Sodium Handling in the Kidney
  • Disorders of serum sodium are water handling problems
  • Disorders of ECF volume are sodium handling problems


List the tubular transporters that are involved in the handling of sodium

  • Na is the most important cation in the body (ECF), and its salts make up >90% of the osmotically active solutes in the ECF
  • Too much Na in the ECF will lead to edema, ascites, etc, while too little will lead to volume contraction
  • ECF Na sensors: Juxtaglomerular apparatus (sense decreased perfusion pressure, as well as sympathetic nerve stimulation) release renin in the case of true or imagined ECF volume contraction too little salt (sodium depletion, diuretics, hemorrhage vs. CHF, cirrhosis, renal artery stenosis)
  • More sensors in heart (ECF excess via atrial and ventricular stretch receptors) to release ANP and BNP, carotid (baroreceptors) change autonomic tone and cardiac output
  • Sodium reabsorption (Na/K/ATPase is involved in almost all parts of the nephron):
    • PCT: symporter with glucose, phosphate and AA; Carbonic Anhydrase prevent loss by making NaHCO3 (<-- CAIs will act here to increase Na loss)
    • Thick Ascending Limb: Na/K/2Cl symport (loop diuretics), affect paracellular Ca movement
    • DCT: Na/Cl symport (thiazides), affect Ca movement through channel
    • CD principal cells: Na channel activity affected by Aldosterone (increase), ANP (decrease). Blocked by K sparing diuretics

Describe how the renin-angiotensin-aldosterone system helps regulate sodium handling by the kidney

  • Angiotensin II:
    • Systemic vasoconstriction, and in the Efferent renal arterioles (increase filtration fraction to push water and salt into nephrons while leaving large proteins to travel to vasa recta, increase peritubular oncotic pressure to draw in water)
    • increase PCT Na cotransporters
    • Increase Aldo production by the adrenals
    • Defending against low ECF volume
  • Aldosterone
    • Increase Na/K/ATPase, esp in cortical collecting duct (all cells), to cause Na retention, K secretion, and alkalosis (by increasing H secretion)
    • Clinical problems: Conn's syndrome, adrenal hyperplasia, Cushing's syndrome, licorice ingestion
    • Defending against low ECF volume
  • ADH
    • Respond to increased osmolality or decreased effective circulating ECF
    • Causes vasoconstriction, increase urea and water reabsorption (aquaporins), increase filtration fraction (increase Na and water reabsorption in the PCT)
    • Defending against low ECF volume
  • Prostaglandings
    • Dilate afferent arteriole to preserve GFR
    • Counterbalance angiotensin II
    • Inhibit Na/K/ATPase throughout the nephron (pee out more water)
    • Defending against high ECF volume
  • Natriuretic peptides
    • Inhibit passive sodium channels in the collecting duct principal cells
    • Defending against high ECF volume


Unless otherwise stated, the content of this page is licensed under Creative Commons Attribution-ShareAlike 3.0 License