Uptake of Zn2+ across the basolateral membrane of the gastric parietal cell is regulated by [Ca2+

Abstract

Aims: Our recent work has suggested that basolateral to apical movement of Zn2+ across the gastric parietal cell (PC) is matched to its secretory state. In this study, we tested the hypothesis that changes in [Ca2+]i may regulate uptake of Zn2+ across the basolateral membrane.Methods: Isolated rabbit gastric glands were loaded with a Zn2+‐sensitive fluorescent dye, fluozin‐3. Cytoplasm loading of Zn2+ in PCs was monitored during a 15 min exposure to solutions containing a “free” [Zn2+] of 10μM. To lower [Ca2+]i, glands were pre‐treated with Ca2+‐free Ringer's (containing 0.3mM EGTA) and thapsigaragin (TG, 2μM), which irreversibly depletes intracellular stores of Ca2+ and opens store‐operated channels (SOCs) that permit Ca2+ to escape from the cytoplasm. To raise [Ca2+]i, glands were pre‐treated with Ca2+‐Ringer's and TG, which permits Ca2+ loading of the cytoplasm through the SOCs.Results and Conclusions: When exposed briefly to Ringer's without TG (n= 21), [Zn2+]i increased 157% ± 2.4 above baseline, indicating PCs have a capacity for Zn2+ uptake. Exposure to Ca2+‐free Ringer's containing TG abolished this response (3.75%± 0.2, n= 42). When exposed to Ca2+‐containing Ringer's and TG, [Zn2+]i increased 60% ± 0.6 (n=25), indicating that extracellular Ca2+ partially restores Zn2+ loading and that uptake of Zn2+ across the basolateral membrane of the PC is regulated by [Ca2+]i.