Inhibition of Ca2+ Entry Caused by Depolarization in Acetylcholine-Stimulated Antral Mucous Cells of Guinea Pig: G Protein Regulation of Ca2+ Permeable Channels.

Nakahari, Takashi; Yoshida, Hideyo; Imai, Yusuke; Fujiwara, Shoko; Ohnishi, Atsuko; Shimamoto, Chikao; Katsu, Ken‐ichi

doi:10.2170/jjphysiol.49.545

Cited by 8 publications

(18 citation statements)

References 15 publications

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“…[ ] i evoked by PGE 2 stimulations were small compared with those evoked by ACh stimulation as previously reported Nakahari et al 1999).…”

Section: Figuresupporting

confidence: 79%

“…The experiments were approved by the Animal Research Committee of Osaka Medical College, and the animals were cared for according to the guidelines of this committee. The procedures for the preparation of cells have been described in detail in previous reports (Nakahari & Imai, 1998;Nakahari et al 1999Nakahari et al , 2000. Briefly, the antrum was excised and the mucosal layer was stripped from the muscle layer in saline at room temperature, using glass slides.…”

Section: Cell Preparationsmentioning

confidence: 99%

“…Our previous report showed that acetylcholine (ACh) increased the frequency of exocytotic events mediated via the [Ca 2+ ] i in antral mucous cells Nakahari et al 1999). On the other hand, prostaglandin E 2 (PGE 2 ) is generally known to be a local chemical mediator that protects the gastric mucosa from acid-peptic injury.…”

mentioning

confidence: 99%

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EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E₂ in Guinea‐Pig Antral Mucous Cells

Ohnishi

Shimamoto

Katsu

et al. 2001

Experimental Physiology

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Effects of prostaglandin E2 (PGE2) on exocytosis of mucin were studied in mucous cells isolated from guinea‐pig antrum using video‐microscopy. Stimulation with PGE2 elicited a sustained increase in the frequency of exocytotic events in a dose‐dependent manner, which was under regulation by both Ca2+ and cAMP. Stimulation with a selective prostanoid EP4 receptor agonist (ONO‐AEI‐329, 10 μM), which activates cAMP signals, elicited a sustained increase in the frequency of exocytotic events (30% of that evoked by 1 μM PGE2). Stimulation with an EP1 agonist (17‐P‐T‐PGE2, 1 μM), which activates Ca2+ signals, increased the frequency of exocytotic events to a lesser extent (5% of that evoked by 1 μM PGE2), while addition of an EP1 antagonist (ONO‐8713, 10 μM) decreased the frequency of exocytotic events (approximately 40% of that evoked by 1 μM PGE2). However, addition of the EP1 agonist potentiated the frequency of exocytotic events evoked by the EP4 agonist or forskolin (which elevates cAMP levels) and increased the sensitivity of the exocytotic events to forskolin. These results suggest that the Ca2+ signal activated via the EP1 receptor potentiates the cAMP‐regulated exocytotic events activated via the EP4 receptor during PGE2 stimulation, by increasing the sensitivity of the exocytotic response to cAMP. In conclusion, exocytotic events in PGE2‐stimulated antral mucous cells were regulated by interactions between EP1 and EP4 receptors.

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“…[ ] i evoked by PGE 2 stimulations were small compared with those evoked by ACh stimulation as previously reported Nakahari et al 1999).…”

Section: Figuresupporting

confidence: 79%

Section: Cell Preparationsmentioning

confidence: 99%

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EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E₂ in Guinea‐Pig Antral Mucous Cells

Ohnishi

Shimamoto

Katsu

et al. 2001

Experimental Physiology

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“…Fura 2-loaded cells were resuspended and stored in solution 1 containing 2% BSA at 4°C and then mounted on a coverslip precoated with neutralized Cell-Tak. These coverslips were set in a perfusion chamber, which was then mounted on the stage of an inverted microscope (IX70, Olympus, Tokyo, Japan) connected to an image analysis system (model ARGUS/HiSCA, Hamamatsu Photonics, Hamamatsu, Japan) (6,19). All the experiments were performed at 37°C.…”

Section: Fig 2 Effect Of CLmentioning

confidence: 99%

“…The DMSO concentration did not exceed 0.1%. At this concentration, DMSO has no effect on cell volume and exocytotic events (6,7,11,15,19,20,(25)(26)(27)(28). Cell preparation.…”

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confidence: 97%

[Cl⁻]_imodulation of Ca²⁺-regulated exocytosis in ACh-stimulated antral mucous cells of guinea pig

Shimamoto¹,

Umegaki²,

Katsu³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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The effects of intracellular Cl− concentration ([Cl−]i) on acetylcholine (ACh)-stimulated exocytosis were studied in guinea pig antral mucous cells by video microscopy. ACh activated Ca2+-regulated exocytosis (an initial phase followed by a sustained phase). Bumetanide (20 μM) or a Cl− -free (NO3−) solution enhanced it; in contrast, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, a Cl− channel blocker) decreased it and eliminated the enhancement induced by bumetanide or NO3− solution. ACh and Ca2+ dose-response studies demonstrated that NO3− solution does not shift their dose-response curves, and ATP depletion studies by dinitrophenol or anoxia demonstrated that exposure of NO3− solution prior to ATP depletion induced an enhanced initial phase followed by a sustained phase, whereas exposure of NO3− solution after ATP depletion induced only a sustained phase. Intracellular Ca2+ concentration ([Ca2+]i) measurements showed that bumetanide and NO3− solution enhanced the ACh-stimulated [Ca2+]i increase. Measurements of [Cl−]i revealed that ACh decreases [Cl−]i and that bumetanide and NO3− solution decreased [Cl−]i and enhanced the ACh-evoked [Cl−]i decrease; in contrast, NPPB increased [Cl−]i and inhibited the [Cl−]i decrease induced by ACh, bumetanide, or NO3− solution. These suggest that [Cl−]i modulates [Ca2+]i increase and ATP-dependent priming. In conclusion, a decrease in [Cl−]i accelerates ATP-dependent priming and [Ca2+]i increase, which enhance Ca2+-regulated exocytosis in ACh-stimulated antral mucous cells.

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[Ca²⁺]_i Oscillations Induced by High [K⁺]_o in Acetylcholine‐Stimulated Rat Submandibular Acinar Cells: Regulation by Depolarization, cAMP and Pertussis Toxin

Yoshida

Marunaka

Nakahari

2003

Experimental Physiology

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Maintaining the extracellular K+ concentration ([K+]o) between 15 and 60 mM induced oscillations in the intracellular Ca2+ concentration ([Ca2+]i) in rat submandibular acinar cells during stimulation with acetylcholine (ACh, 1 μM). These [Ca2+]i oscillations were also induced by 1 μM thapsigargin and were inhibited by 50 μM La3+, 1 μM Gd3+, or the removal of extracellular Ca2+, indicating that the [Ca2+]i oscillations were generated by store‐operated Ca2+ entry (SOC). The frequency of the ACh‐evoked [Ca2+]i oscillations increased from 0.8 to 2.3 mHz as [K+]o was increased from 15 to 50 mM. TEA (an inhibitor of K+ channels) also induced [Ca2+]i oscillations at [K+]o of 4.5 or 7.5 mM in ACh‐stimulated cells. These data suggest that depolarization causes [Ca2+]i to oscillate in ACh‐stimulated submandibular acinar cells. Pertussis toxin (PTX, an inhibitor of G proteins) caused [Ca2+]i to be sustained at a high level in ACh‐stimulated cells at 25 mM or 60 mM [K+]o. This suggests that the [Ca2+]i oscillations are generated by a periodic inactivation of the SOC channels via PTX‐sensitive G proteins, which are stimulated by depolarization. Moreover, in the presence of DBcAMP or forskolin which accumulated cAMP the frequency of the [Ca2+]i oscillations remained constant (approximately 1.2 mHz) when [K+]o was maintained in the range 25‐60 mM. Based on these observations in ACh‐stimulated submandibular acinar cells, we conclude that depolarization stimulates the PTX‐sensitive G proteins, which inactivate the SOC channels periodically ([Ca2+]i oscillation), while hyperpolarization or PTX inhibits the G proteins, maintaining the activation of the SOC channels. Accumulation of cAMP is likely to modulate the PTX‐sensitive G proteins.

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Inhibition of Ca2+ Entry Caused by Depolarization in Acetylcholine-Stimulated Antral Mucous Cells of Guinea Pig: G Protein Regulation of Ca2+ Permeable Channels.

Abstract: Secretory functions in exocrine glands are regulated by intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ). In guinea pig antral mucous cells, the stimulation of acetylcholine (ACh) evoked cell shrinkage followed by exocytotic events, which were regulated by increases in [Ca 2ϩ

Cited by 8 publications

References 15 publications

EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E₂ in Guinea‐Pig Antral Mucous Cells

EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E₂ in Guinea‐Pig Antral Mucous Cells

[Cl⁻]_imodulation of Ca²⁺-regulated exocytosis in ACh-stimulated antral mucous cells of guinea pig

[Ca²⁺]_i Oscillations Induced by High [K⁺]_o in Acetylcholine‐Stimulated Rat Submandibular Acinar Cells: Regulation by Depolarization, cAMP and Pertussis Toxin

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Inhibition of Ca2+ Entry Caused by Depolarization in Acetylcholine-Stimulated Antral Mucous Cells of Guinea Pig: G Protein Regulation of Ca2+ Permeable Channels.

Abstract: Secretory functions in exocrine glands are regulated by intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ). In guinea pig antral mucous cells, the stimulation of acetylcholine (ACh) evoked cell shrinkage followed by exocytotic events, which were regulated by increases in [Ca 2ϩ

Cited by 8 publications

References 15 publications

EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E2 in Guinea‐Pig Antral Mucous Cells

EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E2 in Guinea‐Pig Antral Mucous Cells

[Cl−]imodulation of Ca2+-regulated exocytosis in ACh-stimulated antral mucous cells of guinea pig

[Ca2+]i Oscillations Induced by High [K+]o in Acetylcholine‐Stimulated Rat Submandibular Acinar Cells: Regulation by Depolarization, cAMP and Pertussis Toxin

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EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E₂ in Guinea‐Pig Antral Mucous Cells

EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E₂ in Guinea‐Pig Antral Mucous Cells

[Cl⁻]_imodulation of Ca²⁺-regulated exocytosis in ACh-stimulated antral mucous cells of guinea pig

[Ca²⁺]_i Oscillations Induced by High [K⁺]_o in Acetylcholine‐Stimulated Rat Submandibular Acinar Cells: Regulation by Depolarization, cAMP and Pertussis Toxin