Electrophysiology of Gastric Ion Transport

Demarest, J. R.; Machen, Terry E.

doi:10.1002/cphy.cp060310

Cited by 2 publications

(3 citation statements)

References 101 publications

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“…A number of recent studies in renal epithelial cells and in salivary acinar cells have clearly shown that NH 4 ϩ acts as a surrogate for K ϩ and passes through both the K ϩ channels (3,21) and the Na ϩ -K ϩ -2Cl Ϫ cotransporters (12,20,21), although this has not been examined previously in gastric epithelial cells (8,13). Since the existence of these cation channels has been demonstrated on the basolateral side of the gastric epithelial cells (8,32,33), it seems reasonable to propose that NH 4 ϩ passes through both the K ϩ channel and the Na ϩ -K ϩ -2Cl Ϫ cotransporter on the basolateral surface of gastric epithelial cells, thereby rendering the basolateral membrane more permeable to NH 4 Cl than the apical membrane. This possibility is strongly supported by the present results that the decrease in PD and R induced by the serosal NH 4 Cl was dose-dependently inhibited by serosal BaCl 2 or by serosal bumetanide ( Fig.…”

Section: Discussionmentioning

confidence: 99%

“…First, the difference could be attributable to asymmetrical distribution of the cation channels in highly polarized gastric epithelial cells (8,13). Because ammonia has a pK a of 9.0 (20), calculated [NH 4 ϩ ]:[NH 3 ] at pH 7.4 is ϳ40:1.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that NH 3 , a small lipophilic molecule (molecular weight 17.0), is readily permeable across the phospholipid bilayer of cell membranes in a variety of tissues (19). In contrast, NH 4 ϩ , a monovalent cation, does not diffuse across the cell membrane but does pass through cation channels that are located on the basolateral membrane of the gastric epithelial cells (8,13). Since ammonia has a pK a of 9.0, most of the ammonia exists as NH 4 ϩ under physiological conditions.…”

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confidence: 99%

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Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro

Suzuki

Yanaka

Mizumoto

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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The present study was conducted to elucidate the mechanisms by which Helicobacter pylori (HP)-derived ammonia causes gastric mucosal injury. Intact sheets of guinea pig gastric fundic mucosae were incubated in Ussing chambers. Both the luminal and the serosal pH were kept at 7.4. Transmucosal potential difference (PD) and electrical resistance (R) were monitored as indices of mucosal integrity. Restitution was evaluated by recovery of PD, R, and transmucosal [(3)H]mannitol flux after Triton X-100-induced mucosal injury. The effects of luminal or serosal NH(4)Cl on function and morphology of uninjured or injured mucosae were examined. In uninjured mucosae, serosal NH(4)Cl induced more profound decreases in PD and R and more prominent vacuolation in gastric epithelial cells than did luminal NH(4)Cl. In contrast, luminal NH(4)Cl markedly inhibited restitution in injured mucosae and caused an extensive vacuolation in gastric epithelial cells, as did serosal NH(4)Cl. Transmucosal ammonia flux was greater in the injured than in the uninjured mucosae. These results suggest that 1) basolateral membrane of gastric epithelial cells is more permeable to ammonia than apical membrane and 2) luminal ammonia, at concentrations detected in HP-infected gastric lumen, retards restitution in injured mucosae.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro

Suzuki

Yanaka

Mizumoto

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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pH of TGN and recycling endosomes of H⁺/K⁺-ATPase-transfected HEK-293 cells: implications for pH regulation in the secretory pathway

Machen¹,

Leigh²,

Taylor³

et al. 2003

American Journal of Physiology-Cell Physiology

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The influences of the gastric H+/K+ pump on organelle pH during trafficking to and from the plasma membrane were investigated using HEK-293 cells stably expressing the alpha- and beta-subunits of human H+/K+-ATPase (H+/K+-alpha,beta cells). The pH values of trans-Golgi network (pHTGN) and recycling endosomes (pHRE) were measured by transfecting H+/K+-alpha,beta cells with the pH-sensitive GFP pHluorin fused to targeting sequences of either TGN38 or synaptobrevin, respectively. Immunofluorescence showed that H+/K+-ATPase was present in the plasma membrane, TGN, and RE. The pHTGN was similar in both H+/K+-alpha,beta cells (pHTGN 6.36) and vector-transfected ("mock") cells (pHTGN 6.34); pHRE was also similar in H+/K+-alpha,beta (pHRE 6.40) and mock cells (pHRE 6.37). SCH28080 (inhibits H+/K+-ATPase) caused TGN to alkalinize by 0.12 pH units; subsequent addition of bafilomycin (inhibits H+ v-ATPase) caused TGN to alkalinize from pH 6.4 up to a new steady-state pHTGN of 7.0-7.5, close to pHcytosol. Similar results were observed in RE. Thus H+/K+-ATPases that trafficked to the plasma membrane were active but had small effects to acidify the TGN and RE compared with H+ v-ATPase. Mathematical modeling predicted a large number of H+ v-ATPases (8000) active in the TGN to balance a large, passive H+ leak (with PH approximately 10-3 cm/s) via unidentified pathways out of the TGN. We propose that in the presence of this effective, though inefficient, buffer system in the Golgi and TGN, H+/K+-ATPases (estimated to be approximately 4000 active in the TGN) and other transporters have little effect on luminal pH as they traffic to the plasma membrane.

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Electrophysiology of Gastric Ion Transport

Cited by 2 publications

References 101 publications

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro

pH of TGN and recycling endosomes of H⁺/K⁺-ATPase-transfected HEK-293 cells: implications for pH regulation in the secretory pathway

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Electrophysiology of Gastric Ion Transport

Cited by 2 publications

References 101 publications

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro

pH of TGN and recycling endosomes of H+/K+-ATPase-transfected HEK-293 cells: implications for pH regulation in the secretory pathway

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pH of TGN and recycling endosomes of H⁺/K⁺-ATPase-transfected HEK-293 cells: implications for pH regulation in the secretory pathway