Which of the following is the primary mechanism by which beta-2 adrenergic agonists lower serum potassium in hyperkalemia?

Explanation

## Mechanism of Beta-2 Agonists in Hyperkalemia **Key Point:** Beta-2 adrenergic agonists (e.g., salbutamol, terbutaline) cause a shift of potassium from the extracellular fluid (ECF) into cells, primarily via activation of the Na-K-ATPase pump on muscle and other tissues. ### Cellular Mechanism Beta-2 stimulation → increased intracellular cAMP → activation of Na-K-ATPase → increased uptake of K+ into cells and extrusion of Na+ → net reduction in serum [K+]. **Clinical Pearl:** This is a **transcellular shift**, not true potassium removal from the body. The total body potassium remains unchanged; only the distribution between ECF and ICF is altered. This is why beta-2 agonists are used as **temporary measures** in acute hyperkalemia. ### Why This Is High-Yield | Mechanism | Onset | Duration | Effect on Total K+ | |-----------|-------|----------|-------------------| | Beta-2 agonist (shift) | 10–30 min | 4–6 hours | No change (redistribution) | | Diuretics (renal loss) | 1–2 hours | Sustained | Decreases total K+ | | Cation exchange resins (GI loss) | 4–24 hours | Sustained | Decreases total K+ | **High-Yield:** Beta-2 agonists do NOT increase renal excretion directly—they work by intracellular translocation. Aldosterone (option A) does increase renal K+ loss, but that is not the primary mechanism of beta-2 agonists. [cite:Harrison 21e Ch 280]