Regulation of free cytosolic Ca2+ in the peptic and parietal cells of the rabbit gastric gland.
Quin 2-loaded isolated rabbit gastric glands and purified peptic cells were used to measure free cytosolic Ca2+ ([Ca2+]i) during hormone stimulation. Rabbit gastric glands are composed of peptic and parietal cells with less than 1% endocrine cells. Although both cell types responded to the same hormones, they may be distinguished in terms of the source of Ca2+ bringing about the change in [Ca2+]i. Experiments were designed to assign changes in [Ca2+]i to either the peptic or parietal cells and to attempt to maintain these distinctions in the mixed cell population of gastric glands. It was shown that the peptide cholecystokinin octapeptide induced a rapid and transient increase in [Ca2+]i of isolated peptic cells. This signal was independent of medium Ca2+ and insensitive to the Ca2+ channel blockers La3+ and nifedipine. In gastric glands, the Ca2+ outdependent increase in (Ca2+)i (the secondary transient) was slower and dose dependently blocked by La3+ and nifedipine. This allowed [Ca2+]i levels in the physiologically more intact rabbit gastric glands to be dissected and correlated with fluorescence changes of quin 2 in either cell type. The transient increase in [Ca2+]i coincided with a burst of pepsin but not acid secretion. A subsequent slower phase of pepsin secretion took place while the cells restored near resting [Ca2+]i. Using a combination of the Ca2+ ionophore A23187 and the protein kinase C activating phorbol ester 12-O-tetra-decanoylphorbol 13-acetate, the hormone response pattern of pepsin secretion could be mimicked. The intracellular Ca2+ stores of the peptic cells in the gastric gland remained depleted of Ca2+ until specific antagonists were added. The reloading of intracellular stores required medium Ca2+ although [Ca2+]i was maintained at resting level during the entire reloading period. Hence, a specialized pathway of Ca2+ reloading is postulated.
D000632:Aminopyrine / Q000494:pharmacology; D000634:Aminoquinolines / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001839:Bombesin / Q000494:pharmacology; D003994:Bucladesine / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002122:Calcium Chloride / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D005753:Gastric Mucosa / Q000166:cytology*; D007811:Lanthanum / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010295:Parietal Cells, Gastric / Q000378:metabolism*; D010434:Pepsin A / Q000378:metabolism; D011817:Rabbits; D012844:Sincalide / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000634:Aminoquinolines; D000632:Aminopyrine; D000001:Calcimycin; D003994:Bucladesine; D007811:Lanthanum; D001285:Atropine; D002217:Carbachol; D010434:Pepsin A; D009543:Nifedipine; D012844:Sincalide; D002122:Calcium Chloride; D013755:Tetradecanoylphorbol Acetate; C035739:Quin2; D001839:Bombesin; D002118:Calcium