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Hypertension Quiz

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Which ADH-mediated change directly increases the water permeability of collecting-duct principal cells?

  1. A Removal of aquaporin-2 from the apical membrane
  2. B Dilation of the afferent arteriole
  3. C Insertion of epithelial sodium channels into the apical membrane
  4. D Reduced urea permeability in the inner medullary collecting duct
  5. E Insertion of aquaporin-2 into the apical membrane
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Answer: E. Insertion of aquaporin-2 into the apical membrane

See Antidiuretic Hormone (ADH). ADH increases collecting-duct water permeability by inserting aquaporin-2 channels into the apical membrane (E). Apical means the surface facing the tubular fluid, so the new channels provide a route for water to enter the principal cells lining the duct. ADH acts through V2 receptors and cyclic AMP signalling to promote this channel insertion. Water can then move down the osmotic gradient towards the more concentrated tissues of the kidney, returning to the circulation rather than leaving in urine. The result is a smaller volume of more concentrated urine: ADH changes access to a water pathway rather than directly pumping water against its gradient.

Epithelial sodium channels (C) transport sodium, not water. ADH can increase their activity, so they should not be dismissed as unrelated to the hormone, but they do not directly supply the water channel asked for. Removing aquaporin-2 (A) reduces water permeability, the opposite of ADH's concentrating effect. Afferent arteriolar dilation (B) concerns blood entering the glomerulus, the kidney's filtering capillary tuft, rather than the permeability of collecting-duct cells. D is also opposite to the usual response: ADH increases urea permeability in the terminal inner medullary collecting duct, supporting urine concentration.

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More questions from this set. Start the quiz to answer them and see each explanation.

  1. 1

    Which condition causes hypertension through autonomous adrenal aldosterone secretion that suppresses renin?

  2. 2

    Which renal secretory response links sympathetic nerve activity to activation of the renin–angiotensin–aldosterone system?

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