Reversing hypokalemia with drugs

[ChessMaster3000]

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So I know that B1 receptors are what activate renin, and B2 receptors are what activate the na-k atpase to drive k into cells. If you were to compare an angiotensin receptor blocker, which has effects at blocking aldosterone and therefore reducing k excretion, vs a b1-selective blocker, you would want to pick the ARB to restore K because that is acting a little more directly on the RAAS system (two steps ahead of the B1 blocker). But what if you had a non-selective B-blocker that blocked both B1 and B2? Then when comparing that to either an ACE or ARB, how would you evaluate the relative K sparing effects? Sure the B1 effect is still proximal to the ACE/ARB affect on aldosterone production, but now you have this B2 effect that promotes potassium uptake into cells.

 

[alicealicealice]

Not sure if I understand your question entirely, but pragmatically usually you are correcting hypokalemia in the setting of a patient being total body deficient; therefore you wouldn't want to use a beta blocker to prevent the shift of K into cells, you need to give them more K or stop K excretion. Obviously it depends on the underlying cause, but the the first line is PO repletion or parental if severe; then if refractory or chronic (i.e. patient on a loop) prevent excretion by adding a K sparing diuretic; AFAIK you don't classically use beta blockers in treating hypoK or beta agonist in treating hyperK as it is so indirect and there are better ways.
Theroretically speaking, there are 2 other drivers for the RAAS system besides sympathetic input, namely the macula densa and the JGA sensing volume and salt levels; if RAAS wants to be on for either of those reasons, I don't think a beta blocker will stop it (and may increase it by lowering BP, etc, all depending on the underling cause).