Beta blocker question

Insulin stimulates the movement of potassium inside of cells. Beta blockers cause hyperkalemia b/c they inhibit the secretion of insulin. With no insulin secretion, a masked hypoglycemia and hyperkalemia occur. Therefore the antidotes for beta blocker toxicity consist of glucagon and calcium gluconate. For the hypoglycemia and hyperkalemia respectively.

hope this helps

While what you say is correct, I am not sure that it is the chief mechanism behind beta blockers and serum K+ rise, at least not acutely. It would certainly impact a chronic beta blockade.

Beta receptors are specifically linked to calcium-gated potassium channels, and their activation allows potassium to enter the cell directly. A blocker, therefore, will inhibit this uptake.

This is why giving albuterol can acutely affect the serum K+ level, without having to rely on insulin release.

I know this is a pretty old thread...(9 years old) but hey, I'll give it a go...
JG cells have Beta 1 receptors and they secrete Renin...if you give a selective Beta blocker like Propranolol, then you inhibit Renin secretion from the JG cells which will: -> decrease angiotensin I -> this will then decreases angiotensin II -> which decreases aldosterone...from the Z.Glomerulosa...causing low aldosterone -> which will then cause low sodium -> HIGH POTASSIUM & increased Hydrogen retention...(acidosis).

So you can also say that the use of cardio selective beta blockers can cause: hyponatremia, hyperkalemia & a metabolic acidosis...but, this is obviously just for the sake of learning the big picture in physiology...
You can also turn these results the other way...
HIGH RENIN = HIGH ANGIO I = HIGH ANGIO II = HIGH ALDO = HIGH Na+ = LOW K+ & LOW H+
(alkalosis)
when it comes down to it, I'm sure that the changes are not quite as drastic, but you get the picture...