Effects of bicarbonate and pH on chloride transport by gastric mucosa

1982 ◽  
Vol 243 (1) ◽  
pp. G60-G68 ◽  
Author(s):  
E. C. Manning ◽  
T. E. Machen
Keyword(s):  
Gastric Mucosa ◽  
Intracellular Ph ◽  
Chloride Transport ◽  
Short Circuit ◽  
Ph Dependence ◽  
Short Circuit Current ◽  
Extracellular Ph ◽  
Solution Ph ◽  
Ph Changes

HCO3 and pH dependence of net Cl transport (JClnet) by resting (metiamide-treated) frog gastric mucosa has been investigated in vitro by measuring short-circuit current (Isc = JClnet) and transepithelial conductance (G). With either 100% O2 or 95% O2-5% CO2 gassing, HCO3-free solutions caused large (greater than 50%) reductions in Isc and G. Increases in [HCO3] of the serosal, but not mucosal, solution caused increases in Isc and G. At least part of the effect appeared to be due specifically to the HCO3 moiety, as opposed to the pH changes that also occurred. In HCO3-free solutions (100% O2), increasing serosal solution pH above 7 with either permeable or impermeable buffers caused Isc and G to increase; permeable buffers were somewhat more effective than impermeable buffers. Measurements of intracellular pH (pHc) with [14C]DMO or [14C]methylamine showed that increases in extracellular pH (pHo) caused increases in cellular pH (pHc), and these changes in pHc were independent of buffer type. We conclude that HCO3 and/or high pHo stimulate Isc and G and that buffer permeability and cellular concentration can also affect transport.

Role of nutrient HCO3(-) in protection of amphibian gastric mucosa

1980 ◽  
Vol 239 (6) ◽  
pp. G536-G542
Author(s):  
R. Schiessel ◽  
A. Merhav ◽  
J. B. Matthews ◽  
L. A. Fleischer ◽  
A. Barzilai ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Experimental Conditions ◽  
Slow Decline ◽  
Alkaline Tide ◽  
Artificial Gastric Juice ◽  
Rapid Drop

In in vitro bullfrog fundic mucosa inhibited with 10(-3) M metiamide and exposed to a luminal pH of 2 a progressive slow decline in potential difference (PD) and short-circuit current (Isc) and a rise in resistance (R) were observed when the nutrient solution (N) contained 18 mM HCO3(-), but these changes were restored by an N containing 50 mM HCO3(-). Substitution of PO4(3-) or N-tris(hydroxymethyl)-methyl-2-aminoethanesulfonic acid for NHO3(-) in N caused a rapid drop in PD and Isc in inhibited tissues, changes that could be prevented by 10(-4) M histamine. Ulceration occurred more frequently in metiamide-inhibited gastric sacs exposed to artificial gastric juice with an N of 18 mMHCO3(-) than with 50 mM HCO3(-), but histamine prevented ulceration in the 18 mM HCO3(-) solution. JnetCl approximated Isc under most experimental conditions in inhibited mucosa and was reduced dramatically as were both Jn leads to sCl and Js leads to nCl when HCO3(-) was removed from N. In histamine-stimulated tissues, removal of nutrient HCO3(-) did not influence Cl- transport. Our results are consistent with the proposal that HCO3(-) in N supports normal Cl- flux and that the alkaline tide of actively secreting oxyntic cells can do the same in the absence of ambient HCO3(-).

Effects of ammonium ion and ammonia on function and morphology of in vitro frog gastric mucosa

1993 ◽  
Vol 265 (2) ◽  
pp. G277-G288 ◽  
Author(s):  
A. Yanaka ◽  
H. Muto ◽  
S. Ito ◽  
W. Silen
Keyword(s):  
Gastric Mucosa ◽  
Electrical Resistance ◽  
Rana Catesbeiana ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ammonium Ion ◽  
Gastric Epithelial Cells ◽  
Sudden Drop ◽  
Oxynticopeptic Cells

The effects of ammonium ion (NH+4) and ammonia (NH3) on function and morphology of gastric epithelial cells were studied in intact sheets of in vitro frog (Rana catesbeiana) gastric mucosa. Luminal 115 mM NH4Cl at luminal pH 8.0 (calculated [NH3] 2.7 mM), but not at 5.0 (calculated [NH3] 3 microM) induced 1) an increase in intracellular pH (pHi) in oxynticopeptic cells (OPC) and decreases in transmucosal potential difference (PD) and electrical resistance (R) in resting tissues, 2) a decrease in histamine-stimulated H+ secretion and an increase in H+ backdiffusion after removal of luminal NH4Cl, and 3) augmented acidification of OPC during luminal acidification. Serosal 30 mM NH4Cl at serosal pH 7.2 (calculated [NH3] 0.47 mM) induced 1) an increase in pHi in OPC and inhibition of the alkalinization of OPC after removal of ambient Cl-, 2) a decrease in PD associated with the increase in R and decrease in short-circuit current, effects attenuated by serosal 15 mM K+, accentuated by 0.2 mM Ba2+, and abolished by removal of ambient Cl-, 3) a sudden drop of PD in resting, but not in stimulated tissues, effects prevented by high serosal pH (7.8), serosal HCO3-, or removal of luminal Cl-, 4) a decrease in histamine-stimulated H+ secretion and an increase in H+ backdiffusion after removal of NH4Cl, and 5) augmented acidification of OPC during luminal acidification. These results suggest that 1) luminal NH3, but not NH+4, increases backdiffusion of H+ from the lumen to the mucosa, 2) serosal NH3 and/or NH+4 induces depolarization of OPC and decreases electrogenic Cl- transport, thereby attenuating the activity of the basolateral Cl(-)-HCO3- exchanger in OPC, and 3) both of these effects contribute to the augmented acidification of OPC during exposure to high luminal [H+].

Effect of acetazolamide on sodium and chloride transport by in vitro rabbit ileum

1975 ◽  
Vol 228 (6) ◽  
pp. 1808-1814 ◽  
Author(s):  
HN Nellans ◽  
RA Frizzell ◽  
SG Schultz
Keyword(s):  
Cyclic Amp ◽  
Chloride Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Direct Interaction ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Membrane Component ◽  
Rabbit Ileum

Acetazolamide (8 mM) aboishes active Cl absorption and inhibits but does not abolish active Na absorption by stripped, short-circuited rabbit ileum. These effects are not accompanied by significant changes in the transmural electrical potential difference or short-circuit current. Studies of the undirectional influxes of Na andCl indicate that acetazolamide inhibits the neutral, coupled NaCl influx process at the mucosal membranes. This action appears to explain the observed effect of acetazolamide on active, transepithelial Na and Cl transport. Acetazolamide did not significantly inhibit either spontaneous or theophylline-induced Cl secretion by this preparation, suggesting that the theophylline-induced secretion may not simply be due tothe unmasking of a preexisting efflux process when the neutral influx mechanism is inhibited by theophylline. Finally, inhibition of the neutral NaCl influx process by acetazolamide does not appear to be attributable to an inhibition of endogenous HCO3production or an elevation in intracellular cyclic-AMP levels. Instead, it appearstheat the effect of acetazolamide is due to a direct interaction with a membrane component involved in the coupled influx process.

scholarly journals THE INHIBITORY EFFECT OF STROPHANTHIDIN ON SECRETION BY THE ISOLATED GASTRIC MUCOSA

1959 ◽  
Vol 42 (6) ◽  
pp. 1233-1239 ◽  
Author(s):  
I. L. Cooperstein
Keyword(s):  
Gastric Mucosa ◽  
Chloride Transport ◽  
Short Circuit ◽  
Membrane Conductance ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Transport Systems ◽  
Anion Secretion ◽  
Diffusion Component ◽  
Sodium And Potassium

The unidirectional fluxes of Na+ and Cl- were measured across the isolated gastric mucosa of the bullfrog (R. catesbiana). The addition of strophanthidin, a cardiac aglycone, resulted in marked reductions of the spontaneous potential and short-circuit current. Associated with these changes, the isolated gastric mucosa ceased secreting chloride and hydrogen ion. Although the active component of chloride transfer was inhibited, the exchange diffusion component seemed to increase. No significant changes in membrane conductance or sodium flux were noted. Possible mechanisms of strophanthidin inhibition were discussed in view of its effect on chloride transport across the gastric mucosa and on sodium and potassium transfer in other tissues. It was concluded that the cardiac glycosides may not be specific inhibitors of sodium and potassium transport. This non-specific inhibition suggests that active chloride transport is affected by strophanthidin directly and/or anion secretion is dependent upon normal functioning of cation transport systems in the tissue.

Failure of 16,16-dimethyl PGE2 to prevent inhibitory effect of ethanol on sodium transport in canine gastric mucosa

1985 ◽  
Vol 248 (3) ◽  
pp. G299-G306
Author(s):  
T. A. Miller ◽  
J. M. Henagan ◽  
Y. J. Kuo ◽  
L. L. Shanbour
Keyword(s):  
Gastric Mucosa ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Gastric Epithelium ◽  
Bathing Solution ◽  
Inhibitory Effects ◽  
Stimulation Of

By use of an in vitro canine gastric mucosal preparation, we evaluated the effects of ethanol (2, 4, 6, and 8%, vol/vol) and indomethacin (2.2 X 10(-4)M), with and without 16,16-dimethyl PGE2 pretreatment, on net sodium transport (JNanet) (mucosal to serosal) across gastric epithelium. Although administration of 2 or 4% ethanol to the mucosal bathing solution had no appreciable inhibitory effects on sodium transport, 6 and 8% ethanol and indomethacin significantly inhibited JNanet when compared with untreated control mucosa. This effect was accompanied by inhibition of transmucosal potential difference (PD) and short-circuit current (Isc). In other mucosae exposed to dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution, significant increases in JNanet, PD, and Isc were noted when compared with control mucosa. Addition of 6 or 8% ethanol to the mucosal solution of dimethyl PGE2-pretreated tissue resulted in significant decreases in PD, Isc, and JNanet below control values that were not significantly different from mucosa exposed to 6 and 8% ethanol without PG pretreatment. When indomethacin was added to the mucosal solution following dimethyl PGE2 pretreatment, only slight decreases in PD and Isc below control levels were observed, and the inhibitory effects on JNanet induced by indomethacin without such treatment were abolished. These findings suggest that stimulation of JNanet by prostaglandin may play a role in its ability to prevent indomethacin damage to gastric epithelium but does not appear to be of importance in mediating protection against ethanol damage.

Sodium and chloride transport in the isolated intestine of the earthworm, Lumbricus terrestris (L.)

1982 ◽  
Vol 97 (1) ◽  
pp. 197-216
Author(s):  
J. C. Cornell
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Lumbricus Terrestris ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Ionic Basis ◽  
Good Agreement

1. Measurements of electrical potential difference (PD), short-circuit current (SCC) and unidirectional fluxes of sodium and chloride were made across portions of the intestine. Based on the results, the intestine can be divided into at least four physiologically distinct regions. 2. These four physiological regions, designated from anterior to posterior as R I-II, R III A, R III B and R IV, do not completely correspond to the four anatomically distinct regions of the intestine. 3. The PD (serosal side positive) in R I-II, R III A, R III B and R IV is 1.08, 12.4, 5.61 and 31.7 mV, respectively. 4. The SCC in these same regions is 9.9, 50.4, 49.7, and 16.4 micro A cm2, respectively. 5. When short-circuited, net sodium and net chloride fluxes in the above regions are −0.36 and −0.27, 1.46*** and −0.92*, 1.74*** and −0.06 and 1.01*** and 0.07 mumol cm-2 h-1, respectively. Positive fluxes indicate net mucosal to serosal movements and asterisks indicate significant net fluxes (* P less than 0.05, *** P less than 0.001). 6. There is good agreement between the SCC and net sodium transport in R III B. In the other regions of the intestine the ionic basis of the SCC has not been completely explained. 7. The properties of the intestine in vitro appear to make the intestine well suited for the task of conserving sodium, a function which the intestine performs in vivo.

Hormonal control of chloride transport across locust rectum

1978 ◽  
Vol 56 (8) ◽  
pp. 1879-1882 ◽  
Author(s):  
J. Spring ◽  
J. Hanrahan ◽  
J. Phillips
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Fold Increase ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Hormonal Control ◽  
Net Flux ◽  
Hemolymph Volume ◽  
Camp Levels

Rates of ion transport across locust recta were monitored in vitro by following fluxes of 22Na+ and 36Cl−, short-circuit current (Isc), and open-circuit electropotential difference (PD) across this epithelium for several hours. Corpora cardiaca (CC) homogenates, cAMP, theophylline, and hemolymph of recently fed locusts all stimulate electrogenic transport of Cl− across locust rectum, as indicated by a two- to three-fold increase in 36Cl− net flux, Isc, and PD. Cyclic AMP caused a Cl-dependent increase in PD across the lumen-facing but not the hemocoel-facing plasma membrane of the epithelial cells. We propose that a blood-borne factor, possibly from the CC, causes an elevation in cAMP levels in rectal tissue and that this second messenger acts by increasing Cl− entry into the cell from the rectal lumen. Additional fluid absorption accompanies the resulting increase in transport of NaCl, leading to an increase in the hemolymph volume of previously dehydrated locusts.

Action of 2-deoxy-D-glucose on frog gastric mucosa

1965 ◽  
Vol 209 (3) ◽  
pp. 461-466 ◽  
Author(s):  
George Sachs ◽  
R. Shoemaker ◽  
B. I. Hirschowitz
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Glucose Uptake ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Potential Difference ◽  
Atp Levels

2-Deoxyglucose (2-DG) has been found to inhibit chloride and acid secretion by the in vitro frog mucosa, with a fall in short-circuit current and potential difference and a rise in resistance. The ATP levels and phosphohexoisomerase activity were essentially unchanged following 2-DG treatment. 3-Methyl-O-glucose uptake was reduced by about 50% following preincubation with 2-DG. The O2 consumption was only slightly reduced with 10 mmoles 2-DG, but the CO2 ratio from glucose-6-C14/glucose-1-C14 fell from 0.98 to 0.37, indicating activation of the hexosemonophosphate (HMP) shunt.

Effect of imidazoles on active transport by gastric mucosa and urinary bladder

1965 ◽  
Vol 208 (6) ◽  
pp. 1183-1190 ◽  
Author(s):  
Darwin Alonso ◽  
Richard Rynes ◽  
John B. Harris
Keyword(s):  
Gastric Mucosa ◽  
Urinary Bladder ◽  
Competitive Inhibition ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Buffering Capacity ◽  
Toad Urinary Bladder ◽  
Inhibitory Effects ◽  
Active Sodium

Studies were undertaken to determine whether the stimulatory effect of histamine and the methyl xanthines on the frog gastric mucosa in vitro could be ascribed to the imidazole component of these compounds. The actively transported ions of gastric secretion appear in the form of hydrochloric acid and of a nonacid chloride component that is responsible for the short-circuit current (Isc). At 10–2 m, imidazole reduced acid secretion (Jh) by 80%, which was somewhat greater than the reduction produced by thiocyanate. N-methylimidazole, 2-methylimidazole, 4(5)-methylimidazole, and benzimidazole abolished Jh. The Isc tended to rise as Jh fell. In stimulated mucosae, imidazole and N-methylimidazole promptly reduced oxygen consumption (qO2) by 25%; thiocyanate had a delayed and lesser effect. Pyrazole, 4-hydroxymethylimidazole, and tris had little or no effect on Jh, Isc, or qO2. Imidazole and N-methylimidazole reduced active sodium transport by the toad urinary bladder by 50%. The results indicate that the inhibitory effects of the imidazoles cannot be ascribed to their buffering capacity or to competitive inhibition of histamine. Instead the effects may result from depletion of tissue content of adenosine-3',5'-phosphate or from interference with protein-bound phosphohistidine in oxidative phosphorylation.

Oxygen consumption and active transport of ions by isolated frog gastric mucosa

1963 ◽  
Vol 204 (5) ◽  
pp. 812-816 ◽  
Author(s):  
J. G. Forte ◽  
R. E. Davies
Keyword(s):  
Oxygen Consumption ◽  
Gastric Mucosa ◽  
Chloride Transport ◽  
Short Circuit ◽  
Membrane Conductance ◽  
Short Circuit Current ◽  
Chloride Ions ◽  
Total Oxygen ◽  
Ph Stat ◽  
Stat Method

Isolated bullfrog gastric mucosae were suspended between two glass chambers and bathed with physiological salt solutions equilibrated with 5% CO2 and 95% O2. The transmucosal potential difference, short-circuit current and membrane conductance were measured. Oxygen consumption was measured polarographically and the rate of acid secretion was determined by the pH stat method. Values for the ratio of hydrogen ions secreted to the total oxygen molecules consumed were calculated for 84 experiments and yielded a mean ratio of 1.86 ± 0.51 (sd) with none of the values above 3.5. The ratio of chloride ions transported (calculated as short-circuit current of chloride ions plus hydrochloric acid) to total oxygen consumed for 84 experiments was found to be above 4.0 in 40% of the cases measured (mean 3.80 ± 0.68). A simple redox-pump hypothesis, with molecular oxygen as the electron acceptor, and with one ion moved for each electron transmitted is ruled out as the only operating mechanism to account for active chloride transport by frog gastric mucosa.

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