Calcium involvement in the muscarinic response of the gastric parietal cell

The influence of extracellular Ca 2+ on the mediation of carbachol stimulation in isolated rabbit gastric parietal cells was studied. Removing Ca 2+ from extracellular medium caused a 42% decrease of the aminopyrine accumulation due to carbachol with the same EC 50 value (∼ 5 μM). A short time deple...

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Veröffentlicht in:Cellular signalling 1990, Vol.2 (2), p.177-186
Hauptverfasser: Leonard, A., Guillon, G., Choquet, A., Bali, J.P.
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container_start_page 177
container_title Cellular signalling
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creator Leonard, A.
Guillon, G.
Choquet, A.
Bali, J.P.
description The influence of extracellular Ca 2+ on the mediation of carbachol stimulation in isolated rabbit gastric parietal cells was studied. Removing Ca 2+ from extracellular medium caused a 42% decrease of the aminopyrine accumulation due to carbachol with the same EC 50 value (∼ 5 μM). A short time depletion in extracellular calcium suppressed the carbachol-dependent Ca 2+ influx without affecting Ca 2+ release from internal stores (fura-2 measurements). Similarly, the production of inositol phosphates under cholinergic stimulation was reduced by 29%. A rapid increase in Ins(1, 4, 5)P 3 was obtained 5 s after carbachol stimulation, and this increase was not changed in Ca 2+-dependent medium. In contrast, a 20 min incubation with carbachol caused a 50% reduction in both basal and carbachol-stimulated inositol phosphate accumulations. In conclusion, phospholipase C activation, intracellular Ca 2+ release and aminopyrine accumulation were sequentially observed following carbachol stimulation of the isolated gastric parietal cell and extracellular calcium contributed to sustain this acid secretory response.
doi_str_mv 10.1016/0898-6568(90)90021-2
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Removing Ca 2+ from extracellular medium caused a 42% decrease of the aminopyrine accumulation due to carbachol with the same EC 50 value (∼ 5 μM). A short time depletion in extracellular calcium suppressed the carbachol-dependent Ca 2+ influx without affecting Ca 2+ release from internal stores (fura-2 measurements). Similarly, the production of inositol phosphates under cholinergic stimulation was reduced by 29%. A rapid increase in Ins(1, 4, 5)P 3 was obtained 5 s after carbachol stimulation, and this increase was not changed in Ca 2+-dependent medium. In contrast, a 20 min incubation with carbachol caused a 50% reduction in both basal and carbachol-stimulated inositol phosphate accumulations. 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In conclusion, phospholipase C activation, intracellular Ca 2+ release and aminopyrine accumulation were sequentially observed following carbachol stimulation of the isolated gastric parietal cell and extracellular calcium contributed to sustain this acid secretory response.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>2400633</pmid><doi>10.1016/0898-6568(90)90021-2</doi><tpages>10</tpages></addata></record>
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subjects acid secretion
Aminopyrine - metabolism
Animals
Calcium
Calcium - metabolism
Carbachol - pharmacology
Cells, Cultured
Chromatography, High Pressure Liquid
Dose-Response Relationship, Drug
fura-2
inositol phosphates
Inositol Phosphates - metabolism
Kinetics
muscarinic receptor
parietal cell
Parietal Cells, Gastric - metabolism
rabbit
Rabbits
Receptors, Muscarinic - metabolism
title Calcium involvement in the muscarinic response of the gastric parietal cell
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