Intracellular Activation Events for Parietal Cell Hydrochloric Acid Secretion

Chew, Catherine S.

doi:10.1002/cphy.cp060313

Cited by 3 publications

(4 citation statements)

References 115 publications

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“…The latter was also inhibited by diamine oxidase in the medium (20). Isolated parietal cells respond to histamine with an increase in both cAMP and calcium (8). They also respond to carbachol via a calcium signaling pathway because of the presence of an M 3 receptor subtype on the parietal cell (30,35,41).…”

Section: Discussionmentioning

confidence: 99%

Regulation of parietal cell calcium signaling in gastric glands

Athmann

Zeng

Scott

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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The ligands interacting with enterochromaffin-like (ECL) and parietal cells and the signaling interactions between these cells were investigated in rabbit gastric glands using confocal microscopy. Intracellular calcium concentration ([Ca(2+)](i)) changes were used to monitor cellular responses. Histamine and carbachol increased [Ca(2+)](i) in parietal cells. Gastrin (1 nM) increased [Ca(2+)](i) in ECL cells and adjacent parietal cells. Only the increase of [Ca(2+)](i) in parietal cells was inhibited by H(2) receptor antagonists (H(2)RA). Gastrin (10 nM) evoked an H(2)RA-insensitive [Ca(2+)](i) increase in parietal cells. Carbachol produced large H(2)RA- and somatostatin-insensitive signals in parietal cells. Pituitary adenylate cyclase-activating peptide (PACAP, 100 nM) elevated [Ca(2+)](i) in ECL cells and adjacent parietal cells. H(2)RAs abolished the PACAP-stimulated [Ca(2+)](i) increase in adjacent parietal cells. Somatostatin did not inhibit the increase of [Ca(2+)](i) in parietal cells stimulated with histamine, high gastrin concentrations, or carbachol but abolished ECL cell calcium responses to gastrin or PACAP. Hence, rabbit parietal cells express histaminergic, muscarinic, and CCK-B receptors coupled to calcium signaling but insensitive to somatostatin, whereas rabbit and rat ECL cells express PACAP and CCK-B calcium coupled receptors sensitive to somatostatin.

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Section: Discussionmentioning

confidence: 99%

Regulation of parietal cell calcium signaling in gastric glands

Athmann

Zeng

Scott

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Isolated gastric glands have been widely used as a model of parietal cell function, typically using the uptake of the weak base aminopyrine (AP) as an index of the secretory response to secretagogues (2). For gastric glands freshly isolated from rabbit stomach, the most potent secretagogues are those that evoke secretion via the protein kinase A (PKA) pathway, e.g., dibutyryl-adenosine 3Ј,5Ј-cyclic monophosphate (cAMP), forskolin, or histamine, operating through a G s -coupled H 2 receptor, plus phosphodiesterase inhibitors (6,7). Earlier studies from our laboratory demonstrated the utility of the ␣-toxin-permeabilized gastric gland model to evaluate second messenger pathways in parietal cell secretion (35,38), and these have essentially been confirmed by the recent report of Miller and Hersey (24).…”

mentioning

confidence: 99%

Nucleotide metabolism by gastric glands and H⁺-K⁺-ATPase-enriched membranes

Rong

Utevskaya

Ramilo

et al. 1998

American Journal of Physiology-Gastrointestinal and Liver Physi

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α-Toxin-permeabilized gastric glands represent a functional model in which acid secretion can be elicited by either adenosine 3′,5′-cyclic monophosphate (cAMP) or ATP, with proven morphological and functional transition between resting and secretory states [X. Yao, S. M. Karam, M. Ramilo, Q. Rong, A. Thibodeau, and J. G. Forte. Am. J. Physiol. 271 ( Cell Physiol. 40): C61–C73, 1996.] In this study we use α-toxin-permeabilized rabbit gastric glands to study energy metabolism and the interplay between nucleotides to support acid secretion, as indicated by the accumulation of aminopyrine (AP). When permeabilized glands were treated with a phosphodiesterase inhibitor, the secretory response to cAMP was inhibited, whereas the secretory response to ATP was potentiated. This implied that 1) ATP provided support not only as an energy source but also as substrate for adenylate cyclase, 2) activation of acid secretion by cAMP needed ATP, and 3) ATP and cAMP exchanged rapidly inside parietal cells. To address these issues, we tested the action of adenine nucleotides in the presence and absence of oxidizable substrates. All adenine nucleotides, including AMP, ADP, ATP, and cAMP, could individually enhance the glandular AP accumulation in the presence of substrates, whereas only a high concentration of ATP (5 mM) was able to support secretory activity in substrate-free buffer. Moreover, ATP could maintain 75–80% of maximal secretory activity in phosphate-free buffer; cAMP alone could not support secretion in phosphate-free buffer. In glands and in H+-K+-adenosinetriphosphatase-rich gastric microsomes, we showed the operation of adenylate kinase, creatine kinase, and ATP/ADP exchange activities. These enzymes, together with endogenous adenylate cyclase and phosphodiesterase, provide the recycling of nucleotides essential for the viability of α-toxin-permeabilized gastric glands and imply the importance of nucleotide recycling for energy metabolism in intact parietal cells.

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“…Είναι γενικά παραδεκτό 3 ότι η υπερέκκριση υδροχλωρικού οξέος (υπερχλωρυδρία) που παράγεται από τα καλυπτήρια κύτταρα του σώματος και του θόλου του στομάχου (parietal cells) είναι η κύρια γενεσιουργός αιτία του 12δακτυλικού έλκους.…”

Section: γενικο μεροςunclassified

“…Στη χρόνια γαστρίτιδα υπάρχει μια αυξημένη έκφραση του εκκριτικού στοιχείου 33 πιθανότατα pari passu με τον αυξημένο αριθμό των ανοσοκυττάρων (πλασματοκυττάρων). Το επιθήλιο στη χρονιά γαστρίτιδα βπίσης δείχνει αυξημένη έκφραση των αντιγόνων ιστοσυμβατότητας τύπου 2 τα οποία μπορούν να ενοχοποιούνται για την αύξηση της άνοσου αντίδρασης 3 1.…”

Section: αιτιοπαθογενεια της χρόνιας και αλκαλικής γαστρίτιδαςunclassified

Μετεγχειρητικη Αλκαλικη Γαστριτιδα Μετα Απο Στελεχιαια Βαγοτομη

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Intracellular Activation Events for Parietal Cell Hydrochloric Acid Secretion

Cited by 3 publications

References 115 publications

Regulation of parietal cell calcium signaling in gastric glands

Regulation of parietal cell calcium signaling in gastric glands

Nucleotide metabolism by gastric glands and H⁺-K⁺-ATPase-enriched membranes

Μετεγχειρητικη Αλκαλικη Γαστριτιδα Μετα Απο Στελεχιαια Βαγοτομη

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Intracellular Activation Events for Parietal Cell Hydrochloric Acid Secretion

Cited by 3 publications

References 115 publications

Regulation of parietal cell calcium signaling in gastric glands

Regulation of parietal cell calcium signaling in gastric glands

Nucleotide metabolism by gastric glands and H+-K+-ATPase-enriched membranes

Μετεγχειρητικη Αλκαλικη Γαστριτιδα Μετα Απο Στελεχιαια Βαγοτομη

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Nucleotide metabolism by gastric glands and H⁺-K⁺-ATPase-enriched membranes