
Originally Posted by
ebjack
All beta-2 agonists (clenbuterol, albuterol) cause a drop in serum potassium by moving extracellular potassium into the cell...
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Burton D Rose, MD
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INTRODUCTION — Catecholamines have potentially important clinical effects on potassium balance, primarily by influencing the distribution of potassium between the extracellular fluid and the cells. In particular, stimulation of the ß2-receptors by epinephrine promotes the movement of extracellular potassium into the cells, thereby lowering the plasma potassium concentration [1]; this effect appears to be mediated by increased activity of the cellular Na-K-ATPase pump and possibly by enhanced pancreatic insulin release [2,3]. In comparison, the alpha-receptors tend to impair cell uptake and mildly raise the plasma potassium concentration [4].
One clinical example of this relationship is that the release of epinephrine during a stress response, such as coronary ischemia, delirium tremens, or hypoglycemia, can acutely and transiently lower the plasma potassium concentration by as much as 0.5 to 0.6 meq/L [5-8]. This may be a particular problem in patients with preexisting diuretic-induced mild hypokalemia, in whom the epinephrine effect can reduce the plasma potassium concentration below 2.8 meq/L (show figure 1) [6]. The induction of marked hypokalemia in this setting may contribute to the increase in sudden cardiac death that may be associated with chronic high dose diuretic therapy in patients with hypertension and cardiac disease [9].
A similar hypokalemic effect can be induced by the administration of a ß2-adrenergic agonist, such as albuterol, terbutaline, or dobutamine to treatment asthma or heart failure or to prevent premature labor [10-12]. In heart failure, for example, the acute 0.4 meq/L fall in the plasma potassium concentration can enhance the tendency to ventricular arrhythmias [11].
On the other hand, the ß2-adrenergic effect can be used therapeutically in the initial treatment of severe hyperkalemia, which most often occurs in patients with advanced renal failure. (See "Causes of hyperkalemia"). As an example, preliminary studies suggest that albuterol can transiently lower the plasma potassium concentration in this setting by 0.5 to 1.5 meq/L [13,14]. In comparison, epinephrine has a less predictable potassium-lowering effect in renal failure [14,15]. This difference appears to be related to the alpha-adrenergic (as well as ß2-adrenergic) activity of epinephrine. As mentioned above, activation of alpha-receptors tends to cause potassium movement out of, not into, the cells [4]; for reasons that are unclear, patients with renal failure show increased response to the alpha effect, thereby limiting or even preventing any fall in the plasma potassium concentration [15].