Activation of Apical Chloride Channels in the Gastric Oxyntic Cell

Demarest, J. R.; Loo, Donald D. F.; Sachs, George

doi:10.1126/science.2474200

Cited by 47 publications

(18 citation statements)

References 18 publications

(18 reference statements)

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“…In resting cells that have been incubated in Cl-free solutions and then exposed again to Cl, the rate at which Cl enters the cells (71 mM/min) was approximately equal to the rate of HCO3 loss (measured from the rate of pHi decrease during the initial stages of Cl treatment, calculated to be 81 mM/ min). In the histamine-stimulated cells, when it is expected that the Cl channels in the apical membrane have been activated (Demarest et al, 1989), there was still good agreement between the Cl fluxes (70 mM/min) and the HCO3 fluxes (77 mM/min). In addition, it has been shown previously that 200-500 ,uM H2DIDS largely blocks the Cl-induced changes of pHi (Paradiso et al, 1987), and the present experiments have shown that Cl fluxes were blocked by -80% (Figure 9).…”

Section: Discussionmentioning

confidence: 90%

“…Under these conditions, there will be an inward movement of Cl in exchange for intracellular HCO3. The decrease in Cli compared with the resting cell is likely to be due to the opening of Cl channels in the apical membrane (Demarest et at., 1989), because the decrease of Cli noted during histamine stimulation was not affected by the anion exchanger inhibitor H2DIDS.…”

Section: Discussionmentioning

confidence: 99%

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Regulation of Cl/HCO3 exchange in gastric parietal cells.

Thomas

Machen

1991

Cell Regul

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Microspectrofluorimetry of the fluorescent indicators 2',7'-bis-(2-carboxyethyl)-5(and-6)carboxyfluorescein and 6-methoxy-N -(3-sulfopropyl) -quinolinium was used to measure intracellular pH (pHi), intracellular Cl (Cli), and transmembrane fluxes of HCO3 and Cl in single parietal cells (PC) in isolated rabbit gastric glands incubated in HCOJ C02-buffered solutions. Steady-state pHi was 7.2 in both resting (50 MM cimetidine) and stimulated (100 ,uM histamine) PCs. Transmembrane anion (HCO3 or Cl) flux rates during Cl removal from or readdition to the perfusate were the same in resting and stimulated PCs. These rates increased at alkaline pHi, though this pHi dependence was small in the physiological range. Maximum velocity (Vm,aJ for Cl influx or HCO3 effiux was 80-110 mM/min at pHi 7.6-7.8, and the Km for extracellular concentrations of Cl (Clo) was 25 mM; in the physiological range (pHi 7.1-7.3), V,,,. for anion fluxes was _50 mM/min. Steady-state Cli in the unstimulated PC was 62 ± 5 mM, but on histamine stimulation, Cli decreased rapidly to 25 mM and then increased back to a steady-state level of 44 mM. HCO3 fluxes due to Cl removal or readdition were completely blocked by 0.5 mM 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (H2DIDS), but Cl fluxes were only inhibited by 80%. H2DIDS did not inhibit the decrease in Cli that occurred with histamine treatment. Diphenylamine carboxylate (0.5 mM) inhibited Cl flux by only 50% and caused no additional inhibition of Cl flux when used in conjunction with H2DIDS. Transmembrane anion fluxes during solution Cl removal or readdition occurred 80% through the anion exchanger at the basal membrane and 20% through other pathway(s), presumably the Cl channel in the apical membrane. We conclude that the increase in transport activity via the CI/HCO3 exchanger that occurs during histamine-induced increases in HCI secretion is due mostly to the decrease in Cli. In the resting cell with Cli = 62 mM, Clo = 120 mM, pHi = 7.2, and extracellular pH = 7.4, the anion exchanger is poised near its thermodynamic equilibrium. During histamine stimulation Cli drops from 62 mM to 44 mM, the thermodynamic equilibrium of the anion exchanger at the basolateral membrane is disturbed, and the anion exchanger then exchanges cellular HCO3 for extracellular Cl. Cli serves a crucial regulatory role in stimulus-secretion coupling in the PC.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Regulation of Cl/HCO3 exchange in gastric parietal cells.

Thomas

Machen

1991

Cell Regul

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“…Recently, cyclic AMP-stimulated Cl-channels (12 pS of unit conductance) were found in the apical membrane region of isolated Necturus oxyntic cells (Demarest, Loo & Sachs, 1989). The contribution of this type of Cl-channel to the present wholecell Cl-current can be ruled out; because (1) the power spectra of the Cl-current had only one corner frequency (Fig.…”

Section: Discussionmentioning

confidence: 99%

Arachidonic acid and prostaglandin E2 activate small‐conductance Cl‐ channels in the basolateral membrane of rabbit parietal cells.

Sakai

Okada

Morii

et al. 1992

The Journal of Physiology

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SUMMARY1. C1-channels in the basolateral membrane of non-stimulated parietal cells in isolated rabbit gastric glands were studied by patch-clamp and noise analysis techniques.2. Voltage-independent whole-cell currents were recorded from parietal cells equilibrated with Cl--containing solutions. Upon reducing the Cl-concentration of the basolateral bathing solution, the current-voltage curve was rapidly shifted to the right. The reversal potential changed according to changes in the equilibrium potential for Cl-.3. A Cl-channel blocker, 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) inhibited whole-cell Cl-currents. The half-maximal inhibitory concentration of NPPB was 300,aM, and the inhibition was reversible (at < 200 /tM). Another Cl-channel blocker, 4-acetamido-4'-isothiocyanatostilbene-2,2'-dilsulphonic acid or diphenylamine-2-carboxylate was much less effective.4. The power spectra of whole-cell Cl-current fluctuations contained one Lorentzian component. The single Cl-channel conductance was estimated to be 0 35 pS by the variance noise analysis, which is in agreement with the value obtained by a method of power spectrum analysis (0 29 pS).5. The addition of arachidonic acid (10 /iiM) to the basolateral medium markedly increased the whole-cell Cl-current. The combined application of a cyclo-oxygenase inhibitor, indomethacin (50,uM), and a lipoxygenase inhibitor, esculetin (100 /tM), increased the Cl-current, whereas the administration of a phospholipase A2 inhibitor, mepacrine (100 /tM), significantly decreased the whole-cell Cl-current. 6. A sizeable increase in the whole-cell Cl-current was also induced by a metabolite of arachidonic acid, prostaglandin E2 (10 aM), but not by leukotriene B4

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“…In fact the parietal cells have been shown to secrete HCl with a pH of 0.8 (Demarest et al, 1989). In freshwater rainbow trout (Bucking and Wood, 2009) and seawater steelhead trout (C.B.…”

Section: Introductionmentioning

confidence: 99%

Post-prandial metabolic alkalosis in the seawater-acclimated trout: the alkaline tide comes in

Bucking

Fitzpatrick

Nadella

et al. 2009

Journal of Experimental Biology

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SUMMARYThe consequences of feeding and digestion on acid-base balance and regulation in a marine teleost (seawater-acclimated steelhead trout; Oncorhynchus mykiss) were investigated by tracking changes in blood pH and [HCO 3 -], as well as alterations in net acid or base excretion to the water following feeding. Additionally the role of the intestine in the regulation of acid-base balance during feeding was investigated with an in vitro gut sac technique. Feeding did not affect plasma glucose or urea concentrations, however, total plasma ammonia rose during feeding, peaking between 3 and 24 h following the ingestion of a meal, three-fold above resting control values (~300 μmol ml -1). This increase in plasma ammonia was accompanied by an increase in net ammonia flux to the water (~twofold higher in fed fish versus unfed fish). The arterial blood also became alkaline with increases in pH and plasma [HCO 3 -] between 3 and 12 h following feeding, representing the first measurement of an alkaline tide in a marine teleost. There was no evidence of respiratory compensation for the measured metabolic alkalosis, as Pa CO2 remained unchanged throughout the post-feeding period. However, in contrast to an earlier study on freshwater-acclimated trout, fed fish did not exhibit a compensating increase in net base excretion, but rather took in additional base from the external seawater, amounting to ~8490 μmol kg -1 over 48 h. In vitro experiments suggest that at least a portion of the alkaline tide was eliminated through increased HCO 3 -secretion coupled to Cl -absorption in the intestinal tract. This did not occur in the intestine of freshwater-acclimated trout. The marked effects of the external salinity (seawater versus freshwater) on different post-feeding patterns of acid-base balance are discussed.

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Activation of Apical Chloride Channels in the Gastric Oxyntic Cell

Cited by 47 publications

References 18 publications

Regulation of Cl/HCO3 exchange in gastric parietal cells.

Regulation of Cl/HCO3 exchange in gastric parietal cells.

Arachidonic acid and prostaglandin E2 activate small‐conductance Cl‐ channels in the basolateral membrane of rabbit parietal cells.

Post-prandial metabolic alkalosis in the seawater-acclimated trout: the alkaline tide comes in

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