Intracellular pH measurements in gastric mucosa.

Intracellular pH was measured in bullfrog gastric mucosa using a pH-indicator dye, bromthymol blue (BTB), with a spectrophotometric technique. Studies showed that BTB is taken up by the gastric mucosa and bound to intracellular components. The binding of BTB was shown to cause a shift in the pKa of the dye from the solution value of 6.95 to a value of 8.0. During the nonsecreting state, intracellular pH was estimated to be 7.4 (metiamide inhibition) or 7.1 (SCN inhibition). During active secretion of acid, intracellular pH increased with increasing secretion rates, reaching values in excess of pH 8. Using preparations from which the surface epithelial cells had been removed, it was shown that at least a portion of the alkaline response to stimulation occurs in the oxyntic or tubular cells. The results are interpreted in view of existing models for the chemical reaction involved in gastric acid secretion.

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Evidence for Cl(-)-independent HCO3- transport in basolateral membranes of Necturus oxyntopeptic cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1996.271.6.g1096 ◽

1996 ◽

Vol 271 (6) ◽

pp. G1096-G1103

Author(s):

M. E. Klingensmith ◽

R. R. Cima ◽

A. E. Gadacz ◽

D. I. Soybel

Keyword(s):

Gastric Mucosa ◽

Recent Work ◽

Intracellular Ph ◽

Disulfonic Acid ◽

Substantial Part ◽

Ph Indicator ◽

Basolateral Membranes ◽

Hcl Secretion ◽

Ethanesulfonic Acid

Luminal H+ secretion by gastric mucosa is accompanied by basolateral HCO3- release. A basolateral Cl-/HCO3- exchanger is known to mediate HCO3- extrusion from oxyntopeptic cells during resting and secretagogue-induced apical HCl secretion. From recent work, we hypothesized that there might be a Cl(-)-independent pathway for basolateral HCO3- exit in Necturus oxyntopeptic cells. In this study, we used a fluorescent pH indicator [2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein] to evaluate Cl(-)-independent HCO3- transport across the basolateral membranes of intact oxyntopeptic cells. Removal of serosal Cl- increased intracellular pH (pHi) (7.05 to 7.25), consistent with Cl(-)-dependent HCO3- extrusion. Removal of serosal Na+ in the absence of Cl- resulted in significant acidification of pHi (7.10 to 6.89), but studies involving amiloride, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), and 0 HCO3(-)-N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solutions suggest that Na(+)-dependent changes in pHi are due to Na+/H+ exchange. Our studies demonstrate a marked concentration-dependent alkalinization when tissues are exposed to increases in serosal K+. A substantial part of this alkalinization in response to increases in serosal K+ (pHi 7.00 to 7.46) appears to be a HCO3- exit pathway that is independent of both Na+ and Cl-, unaffected by bumetanide or amiloride, but sensitive to DIDS. We propose the presence of a Cl(-)- and Na(+)-independent K(+)-dependent HCO3- cotransporter in Necturus oxyntopeptic cell basolateral membranes.

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Agonist-specific role for Na+-H+ antiport in prostaglandin release from microvessel endothelium

AJP Cell Physiology ◽

10.1152/ajpcell.1989.256.4.c831 ◽

1989 ◽

Vol 256 (4) ◽

pp. C831-C839 ◽

Cited By ~ 16

Author(s):

M. E. Gerritsen ◽

C. A. Perry ◽

T. Moatter ◽

E. J. Cragoe ◽

M. S. Medow

Keyword(s):

Intracellular Ph ◽

Specific Role ◽

Na Channel ◽

Ionophore A23187 ◽

Ph Indicator ◽

Prostaglandin Release ◽

Human Thrombin ◽

Thrombin Activation ◽

Pg Release ◽

Indicator Dye

Rabbit coronary microvascular endothelial (RCME) cells synthesize prostaglandin (PG) I2 and PGE2 in response to stimulation with human thrombin, ATP, and the Ca2+ ionophore, A23187. Replacement of extracellular Na+ with choline or N-methylglucamine reduced thrombin-stimulated PG secretion but did not significantly affect either ATP- or A23187-stimulated PG secretion. Pretreatment of RCME cells with Na+ channel or Na+ -Ca2+ exchange blockers did not alter PG release in response to any of these three agonists. Pretreatment of RCME cells with the specific Na+ -H+ antiport blockers 5-(N-ethyl-N-isopropyl)-amiloride (EIPA, 10 microM) and 5-(N,N-hexamethylene)-amiloride (HMA, 0.1 microM) significantly reduced thrombin but not A23187- or ATP-stimulated PG secretion. Studies with the intracellular pH indicator dye 2,7-bis(carboxyethyl)-5(6)-carboxyfluorescein demonstrated thrombin activation of Na+ -H+ antiport, an effect blocked by either HMA or EIPA. Since manipulations known to inhibit Na+ -H+ exchange (EIPA, HMA, replacement of Na+ with choline or N-methylglucamine) reduced thrombin-stimulated RCME cell PG release, we conclude that activation of Na+ -H+ exchange is involved in the coupling of thrombin interaction with RCME cells to subsequent phospholipase activation and PG release.

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The energetic coupling of acid secretion in gastric mucosa

Philosophical Transactions of the Royal Society of London Series B Biological Sciences ◽

10.1098/rstb.1971.0092 ◽

1971 ◽

Vol 262 (842) ◽

pp. 261-275 ◽

Cited By ~ 11

Keyword(s):

Gastric Mucosa ◽

Acid Secretion ◽

Intracellular Ph ◽

Respiratory Chain ◽

Oxidative Metabolism ◽

Chloride Secretion ◽

High Energy ◽

Hydrogen Ion ◽

Close Coupling ◽

Ion Secretion

The relation between acid secretion and oxidative metabolism has been investigated using nondestructive optical techniques to monitor the redox level of respiratory chain components in the intact, isolated bull-frog gastric mucosa. High rates of acid secretion are found to be associated with cytochrome reduction while inhibition of secretion results in oxidation of the respiratory chain components. Changes in chloride secretion, independent of hydrogen ion secretion, result in opposite cytochrome redox changes indicating that the interaction with oxidative metabolism differs for the two secretory processes. Measurement of intracellular pH changes using indicator dyes shows a correlation between cytochrome reduction and increased pH. The results suggest that there exists a close coupling between the respiratory chain components and hydrogen ion secretion and that this coupling may involve changes in intracellular pH rather than changes in high energy phosphate compounds as previously suggested.

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Expression of NKCC1 and NKCC2 in gastric mucosa and their possible role in acid secretion

Cell Biology International ◽

10.1042/cbi034s002c ◽

2010 ◽

Vol 34 (8) ◽

pp. S2-S2

Author(s):

Tuo Ji ◽

Hong Xue ◽

Zhangfeng Dou ◽

Yue Zhang ◽

Jinxia Zhu

Keyword(s):

Gastric Mucosa ◽

Acid Secretion

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Green Fluorescent Protein as a Noninvasive Intracellular pH Indicator

Biophysical Journal ◽

10.1016/s0006-3495(98)77870-1 ◽

1998 ◽

Vol 74 (3) ◽

pp. 1591-1599 ◽

Cited By ~ 461

Author(s):

Malea Kneen ◽

Javier Farinas ◽

Yuxin Li ◽

A.S. Verkman

Keyword(s):

Green Fluorescent Protein ◽

Intracellular Ph ◽

Fluorescent Protein ◽

Ph Indicator ◽

Green Fluorescent

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Nitric oxide inhibits gastric acid secretion by increasing intraparietal cell levels of cGMP in isolated human gastric glands

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00230.2005 ◽

2005 ◽

Vol 289 (6) ◽

pp. G1061-G1066 ◽

Cited By ~ 16

Author(s):

Anna Berg ◽

Stefan Redéen ◽

Magnus Grenegård ◽

Ann-Charlott Ericson ◽

Sven Erik Sjöstrand

Keyword(s):

Nitric Oxide ◽

Gastric Mucosa ◽

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Enzymatic Digestion ◽

Human Gastric Mucosa ◽

Gastric Glands ◽

Oxyntic Mucosa ◽

No Donor

We have previously identified cells containing the enzyme nitric oxide (NO) synthase (NOS) in the human gastric mucosa. Moreover, we have demonstrated that endogenous and exogenous NO has been shown to decrease histamine-stimulated acid secretion in isolated human gastric glands. The present investigation aimed to further determine whether this action of NO was mediated by the activation of guanylyl cyclase (GC) and subsequent production of cGMP. Isolated gastric glands were obtained after enzymatic digestion of biopsies taken from the oxyntic mucosa of healthy volunteers. Acid secretion was assessed by measuring [14C]aminopyrine accumulation, and the concentration of cGMP was determined by radioimmunoassay. In addition, immunohistochemistry was used to examine the localization of cGMP in mucosal preparations after stimulation with the NO donor S-nitroso- N-acetylpenicillamine (SNAP). SNAP (0.1 mM) was shown to decrease acid secretion stimulated by histamine (50 μM); this effect was accompanied by an increase in cGMP production, which was histologically localized to parietal cells. The membrane-permeable cGMP analog dibuturyl-cGMP (db-cGMP; 0.1–1 mM) dose dependently inhibited acid secretion. Additionally, the effect of SNAP was prevented by preincubating the glands with the GC inhibitor 4 H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4]oxazin-1-one (10 μM). We therefore suggest that NO in the human gastric mucosa is of physiological importance in regulating acid secretion. Furthermore, the results show that NO-induced inhibition of gastric acid secretion is a cGMP-dependent mechanism in the parietal cell involving the activation of GC.

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Effect of dimethyl sulfoxide applications on gastric secretory function

Kazan medical journal ◽

10.17816/kazmj62008 ◽

1982 ◽

Vol 63 (3) ◽

pp. 24-25

Author(s):

S. G. Vaynshteyn ◽

Yu. V. Afanasyeva ◽

D. H. Maksudova ◽

M. I. Pivikova

Keyword(s):

Gastric Mucosa ◽

Acid Secretion ◽

Dimethyl Sulfoxide ◽

Chronic Gastritis ◽

Secretory Function ◽

Normal Acid

The use of applications of dimethyl sulfoxide in patients with ulcerative disease and chronic gastritis leads to suppression of increased acid secretion, ambivalence with normal acid secretion and has no effect in patients with atrophy of the gastric mucosa. The normalizing effect of dimethyl sulfoxide (DMSO) applications in persons with acidic, decompensated ^ and subcompensated states of the stomach by stimulating the neutralizing function of the antral glands was established. The use of dimethyl sulfoxide as a transporter of various drugs in physiotherapy can be indicated in patients with HC1 hypersecretion in the interdigestive phase of ventricular secretion.

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