ANP mechanism?

[Aclamity]

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pg. 512 of FA says ANP increases Na+ filtration "with NO compensoatory Na+ reabsorption in distal nephron"... anyone know the mechanism for this? How does ANP prevent Na+ reabsorption elsewhere? As far as I know it just dilates the aff arteriole and constricts the eff arteriole. Thx

 

[VisionaryTics]

pg. 512 of FA says ANP increases Na+ filtration "with NO compensoatory Na+ reabsorption in distal nephron"... anyone know the mechanism for this? How does ANP prevent Na+ reabsorption elsewhere? As far as I know it just dilates the aff arteriole and constricts the eff arteriole. Thx

Inhibits renin release.

 

[ijn]

In terms of the mechanism, wiki claims that increased cGMP in the DCT results in phosphorylation and thus inhibition of ENaC.

 

[Phloston]

P. 60 of High-Yield Kidney (yes, I own this book) says, "ANP binds to the NPR-A and NPR-C receptors. The NPR-A receptor is a G-protein-linked receptor. The NPR-C receptor is believed to be a 'decoy receptor' because it lacks an intracellular domain." It then goes on to vaguely say, "ANP acts on the principal cells of the medullary collecting ducts and causes decreased Na+ reabsorption," and that BNP (not ANP) also binds to NPR-A and -C.

Based on what ijn's added regarding the increased intra-principal cell [cGMP], that would actually imply a G-alpha-q protein. I recall from Kaplan QBook that the increased intracellular calcium, as induced by inositol triphosphate, activates guanylate cyclase, thereby increasing cGMP concentrations.

Therefore, increased positive charge within the cell due to Ca2+ would decrease Na+ reabsorption through ENaC, based on diminished charge gradient, the same way that K+ wouldn't move into the lumen when amiloride or triamterene diminish the charge gradient by inhibiting ENaC.

Hope that helps,