What substances enhance the activity of Na/K-ATPase, leading to hypokalemia?

The substances that enhance the activity of Na/K-ATPase, resulting in hypokalemia, are indeed albuterol and insulin.

Albuterol, a beta-2 adrenergic agonist, stimulates Na/K-ATPase activity. This results in an increased uptake of potassium into cells, thereby lowering serum potassium levels, which can lead to hypokalemia. Insulin also promotes the intracellular uptake of potassium, similar to albuterol, by enhancing the activity of Na/K-ATPase. Through this mechanism, both of these substances facilitate the movement of potassium from the extracellular space into cells.

In contrast, while aldosterone increases the reabsorption of sodium and secretion of potassium in the kidneys, it primarily acts at different sites when compared to albuterol and insulin. Aldosterone enhances renal tubular Na/K-ATPase activity but is not a direct stimulant of the activity that leads to immediate hypokalemia in the broader physiological context.

Other options like beta-blockers and succinylcholine do not have a similar effect on Na/K-ATPase to the degree that contributes to hypokalemia. Beta-blockers typically have opposite effects in certain contexts, and succinylcholine can cause hyperkalemia due to potassium release from muscle tissue. Lastly