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 +1  (nbme22#4)

I got that it needed to be a potassium sparing diuretic. Is there a reason it cannot be an aldosterone antagonist? I chose blocks basolateral K+ channels as these decrease the basolateral K+/Na+/ATPase because the wording of the correct answer did not make sense to me -- assuming they were going for an ENaC blocker (and that decreased luminal permeability indicates that Na+ would be remaining in the lumen, not remaining in the principal cell as I originally thought).

luckeroo  I think the reason it’s a potassium-sparing diuretic rather than an aldosterone antagonist has less to do with why the aldosterone antagonist cannot be used and more to do with the fact that a potassium-sparing diuretic would be more of a “first-line” adjunctive diuretic treatment.
luckeroo  As for the answer choice, potassium sparing diuretics achieve their overall anti-aldosterone effect by competitively inhibiting aldosterone receptors on the interstitial side (decreasing the Na/K-ATPase effect of shunting Na into the blood), thereby decreasing the gradient for sodium to enter the cell from the luminal aspect, blocking ENaC.
yotsubato  There is no such thing as "Basolateral K Channel" there is only basolateral Sodium Potassium Pumps which are controlled by aldosterone. FA pg 573
nwinkelmann  @yotsubato LOL.... why didn't I think of it that what?! (by the way, that LOL is for me). The only basolateral K channel is the nephron (based on the first aid picture) is in the thick ascending limb of the loop of henle.
hello  Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase, so I'm not sure what @luckeroo is referring to. Spironolactone and aplerenone are both ALDO antagonists. Na/K ATPase is found on the basolateral membrane. None of the answer choices fit with this. Amiloride and triamterene are also potassium-sparing diuretics; their mechanism is to block ENaC channels on the luminal membrane, this is choice "B."




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