Aquaporin-2 (AQP2) water channels are inserted into the apical membrane of collecting duct principal cells in response to ADH. The second messenger that drives AQP2 vesicle exocytosis is:

• A cAMP via protein kinase A phosphorylation of AQP2 ✓
• B Inositol triphosphate (IP3) via phospholipase C activation
• C cGMP via natriuretic peptide receptor activation
• D Diacylglycerol (DAG) via protein kinase C

Explanation

ADH (vasopressin) binds V2 receptors on collecting duct principal cells, activating adenylyl cyclase via Gs protein to generate cAMP. cAMP activates protein kinase A, which phosphorylates AQP2 at serine-256, triggering exocytotic insertion of AQP2-containing vesicles into the apical membrane. This increases water permeability. V1 receptors (smooth muscle vasoconstriction) use IP3/DAG via Gq. Congenital nephrogenic DI can result from V2 receptor or AQP2 mutations.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.