A 24-year-old asthmatic self-medicates with frequent high-dose salbutamol nebulisations during an acute attack. Repeat electrolytes show serum potassium of 2.9 mEq/L. The mechanism of salbutamol induced hypokalemia is:
- A Beta-2 receptor mediated stimulation of Na-K ATPase, driving potassium into skeletal muscle cells ✓
- B Renal potassium wasting through beta-2 mediated inhibition of aldosterone secretion
- C Insulin release from pancreatic beta cells secondary to beta-3 receptor stimulation
- D Metabolic acidosis causing intracellular shift of potassium
Correct answer: A. Beta-2 receptor mediated stimulation of Na-K ATPase, driving potassium into skeletal muscle cells
Explanation
Beta-2 receptor activation increases cyclic AMP in skeletal muscle, which stimulates cell membrane Na-K ATPase and drives extracellular potassium into cells. This same mechanism underlies the use of nebulised salbutamol as adjunctive therapy in hyperkalemia. The shift is not renal in origin and aldosterone is actually stimulated, not inhibited, by beta-2 activation. Metabolic effects of salbutamol tend toward lactic acidosis, not acidosis driven potassium shift.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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