Carbachol-induced changes in 45Ca fluxes and cytosolic free Ca2+ were characterized in rabbit gastric glands and isolated dog parietal cells. Cholinergic stimulation was expressed as changes in the membrane permeability of the parietal cell to Ca2+ without Ca2+ release from intracellular stores. The changes in the membrane permeability to Ca2+ were sustained as long as the cells were exposed to carbachol, independent of extracellular Ca2+, and had the properties of a passive pathway across which Ca2+ distributed according to its chemical gradient. As a consequence of the changes in membrane permeability to Ca2+, carbachol caused a sustained increase in free cytosolic Ca2+ from a resting level of 134 +/- 11 to 533 +/- 81 nM (n = 14). After carbachol stimulation, calcium ions were sequestered in mitochondrial and probably nonmitochondrial compartments. When cell stimulation was terminated by atropine or La3+, the cells restored the resting level of the intracellular Ca2+ activity ([Ca2+]in), independent of uncoupling of mitochondrial oxidation phosphorylation. Reduction in [Ca2+]in was mainly through Ca2+ efflux across the plasma membrane of the parietal cell. Manipulation of intracellular Na+ ion activity in intact cells and studies with basal-lateral membrane vesicles from gastric mucosa indicated the absence of extracellular Na+-intracellular Ca2+ exchange activity in the plasma membrane of the parietal cell. A calmodulin-regulated, ATP-dependent Ca2+ pump that could maintain active Ca2+ extrusion from parietal cells was found in the basal-lateral membrane of the parietal cells.
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