Calcium release‐activated calcium (CRAC) channels mediate the β2‐adrenergic regulation of Na,K‐ATPase.

β2‐Adrenergic agonists have been shown to regulate Na,K‐ATPase in the alveolar epithelium by recruiting Na,K‐ATPase‐containing vesicles to the plasma membrane of alveolar epithelial cells (AEC). Here, we provide evidence that β2‐agonists induce store‐operated calcium entry (SOCE) in AECs. This calcium entry is necessary for β2‐agonist‐induced recruitment of Na,K‐ATPase to the plasma membrane of AECs. Specifically, we show that β2‐agonists induce SOCE via stromal interaction molecule 1 (STIM1)‐associated calcium release‐activated calcium (CRAC) channels. We also demonstrate that the magnitude of SOCE affects the abundance of Na,K‐ATPase at the plasma membrane of AECs.β2‐Agonists elicit store‐operated Ca2 + entry (SOCE) in alveolar epithelial cells. Ca2+ entry is necessary for the β2‐agonist‐induced upregulation of Na,K‐ATPase. STIM1‐associated CRAC channels mediate the β2‐agonist‐induced SOCE. The magnitude of Ca2+ entry affects the abundance of plasma membrane Na,K‐ATPase. [ABSTRACT FROM AUTHOR]