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Fig. 1. Relationship between intracellular and extracellular [Ca²⁺] changes in polarized gastric epithelial cells. Intracellular inositol (1,4,5)-trisphosphate [Ins(1,4,5)P₃]-sensitive internal stores contain large amounts of Ca²⁺. Stimulation of cells with an Ins(1,4,5)P₃-generating agonist results in the release of Ca²⁺ into the cytoplasm, and a drop in free intraluminal [Ca²⁺] in stores of several hundred µM. The resulting Ca²⁺ spike in the highly buffered cytoplasmic milieu elevates free intracellular [Ca²⁺] from a resting value of 100 nM to 1000 nM. Much of this Ca²⁺ is rapidly extruded by Ca²⁺-export mechanisms, such as the plasma membrane Ca²⁺-ATPase (PMCA) pump, which has an apical localization in these cells. Extracellular [Ca²⁺] in the restricted luminal domain of gastric glands transiently increases by hundreds of µM as a consequence of Ca²⁺ extrusion. Concomitantly, store depletion triggers the opening of store-operated channels (SOCs) in the basolateral plasma membrane and the resulting Ca²⁺ influx depletes extracellular Ca²⁺ in the limited interstitial spaces by several hundred µM (Caroppo et al., 2001; Hofer et al., 2004). When Ins(1,4,5)P₃ production is terminated, reuptake of Ca²⁺ into internal stores mediated by the sarco-endoplasmic reticulum ATPase (SERCA) causes Ca²⁺ entry to cease.

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