Electrophysiology of the frog gastric mucosa with sufficient CO2

1975 ◽  
Vol 228 (3) ◽  
pp. 928-933 ◽  
Author(s):  
Kidder GW

Changing from 5% CO2 in the serosal solution only to 10% CO2 on both sides doubles the acid secretory rate of the bullfrog stomach (as shown previously) and raises the transmural potential difference, although the short-circuit current is not changed. The secretory overshoot on reoxygenation after anaerobiosis, observed in 5% CO2, is virtually eliminated in 10% CO2, as predicted by the diffusion model which explains the secretory rate increase. It was found that the rate of rise of the secretory rate during anoxia was identical in the 2 conditions, which explains the increased secretory lag in 10% CO2 and suggests an interesting limitation on the rate with which acid secretion can be activated. During anoxia in 10% CO2, but not in 5% CO2, there occurs a sudden drop in PD to a slightly negative value associated with a fall in tissue resistance. This effect occurs under SCN-inhibition and thus seems unrelated to H+ transport per se. A working model is presented which can explain some of the events surrounding the sudden potential drop.

1975 ◽  
Vol 228 (2) ◽  
pp. 511-517 ◽  
Author(s):  
PK Rangachari

Ba++ added to the nutrient solution bathing the resting frog stomach increased resistance, decreased the PD, and stimulated acid secretion. Under short-circuit conditions, the increase in H+-secretory rate was accompanied by a decrease in short-circuit current (I-sc). These changes were reversed by NaSCN (10 mM), suggesting that Ba++ had not impaired the current-generating mechanism per se. Histamine-induced acid secretion was associated with an increase in net Cl- flux, particularly in the N yields S flux (JNS). Ba++ increased acid secretion with no increase in JNS and a decrease in net Cl- flux. The effects of Ba++ were amplified by low-Cl- solutions. Histamine, in the presence of Ba++ and low-Cl- solutions, increased acid secretion and transmucosal resistance, suggesting the operation of a neutral pump in the secretion of HCl. It is concluded that Ba++ limits Cl- entry and also acts as a secretagogue.


1962 ◽  
Vol 203 (6) ◽  
pp. 1091-1093 ◽  
Author(s):  
Warren S. Rehm

The present report is concerned with in vitro studies on gastric mucosa of the skate, Raja eglentaria, the electric ray, Narcine braziliensis, and the shark, Negaprion brevirostris. Maximum secretory rates of from 0.65 to 2.7 µEq hr–1 cm–2 were found. An increase in the secretory rate from an initial low level was associated with an increase in potential difference (PD), a decrease in resistance, and an increase in the calculated short-circuit current. The average PD and resistance before the increase in the secretory rate was 2.2 mv (nutrient positive) and 268 ohms cm2. After the increase they were 6.4 mv and 199 ohms cm2. Thiocyanate (10–2 m) to nutrient resulted in a decrease of secretory rate to zero and an increase in PD and resistance. The results can be explained on the basis of the separate mechanisms theory of H+ and Cl– ion secretion on the assumption that the resistance in the Cl– ion limb of the circuit is considerably lower than that in the H+ ion limb of the circuit.


1993 ◽  
Vol 265 (2) ◽  
pp. G277-G288 ◽  
Author(s):  
A. Yanaka ◽  
H. Muto ◽  
S. Ito ◽  
W. Silen

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+].


1985 ◽  
Vol 248 (2) ◽  
pp. G246-G250 ◽  
Author(s):  
S. J. Hersey ◽  
G. Sachs ◽  
D. K. Kasbekar

The action of a newly developed, specific inhibitor of the gastric proton pump, omeprazole, was investigated using intact frog gastric mucosa. Omeprazole was found to inhibit acid secretion, and the inhibition could be reversed with glutathione or 2-mercaptoethanol. Inhibition was not stimulus specific, occurring with histamine, carbachol, and forskolin. With hypertonic solutions bathing the mucosal surface, omeprazole inhibition of acid secretion did not change the tissue conductance, whereas inhibition by thiocyanate or cimetidine resulted in a significant decrease in conductance. With high-K+ (greater than 80 mM) sulfate solutions bathing both surfaces, omeprazole inhibition of acid secretion resulted in no change in transtissue potential difference. In chloride solutions, omeprazole caused an increase in potential difference and short-circuit current. These results provide evidence that the proton pump in frog gastric mucosa is electroneutral.


1965 ◽  
Vol 209 (3) ◽  
pp. 461-466 ◽  
Author(s):  
George Sachs ◽  
R. Shoemaker ◽  
B. I. Hirschowitz

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.


1987 ◽  
Vol 252 (4) ◽  
pp. G543-G547 ◽  
Author(s):  
W. W. Reenstra ◽  
J. D. Bettencourt ◽  
J. G. Forte

Net Cl- flux across the bullfrog gastric mucosa was examined to test the hypothesis that Cl-secretion (JClnet) can be driven by either of the two cation exchange pumps in the oxyntic cell. The effects on JClnet of ouabain, an Na+-K+ pump inhibitor, and omeprazole, an H+-K+ pump inhibitor were examined. Omeprazole abolished acid secretion (JH) and reduced JClnet in bullfrog gastric mucosa. For mucosae at open circuit the omeprazole-induced decrease in JH was not significantly different than the decrease in JClnet, and the transmucosal potential difference (PD) was increased. When short-circuited mucosae were treated with omeprazole, the decrease in JClnet was significantly less than the decrease in JH, and short-circuit current (SCC) was correspondingly increased. After treatment of short-circuited mucosae with ouabain, the omeprazole-induced decreases in JH and JClnet were not significantly different, and no change in SCC occurred. For open-circuited mucosae, pretreatment with ouabain resulted in a significantly smaller omeprazole-induced increase in the transmucosal PD than was seen without ouabain pretreatment. Our data 1) show that both the H+-K+ pump and the Na+-K+ pump can drive Cl- secretion and 2) suggest that inhibition of the H+-K+ pump with omeprazole stimulates the Na+-K+ pump.


1964 ◽  
Vol 206 (1) ◽  
pp. 218-222 ◽  
Author(s):  
J. G. Forte ◽  
R. E. Davies

Bullfrog gastric mucosae were isolated, mounted between two glass chambers, and bathed with physiological salt solutions equilibrated with 5% CO2 and 95% O2. Oxygen consumption (qO2; measured polarographically) and acid secretion (qH+; pH stat method) were measured along with the transmucosal potential difference (p.d.) and current passing through the mucosa. Histamine (4 x 10–4 m) caused an increase in qH+ and qO2. In measurements on nine short-circuited mucosae the mean ratio for the ΔqH+/ΔqO2 was 2.1. Sodium thiocyanate (0.5–15 mm) caused a decrease in qH+ and qO2 and an increase in short-circuit current. These effects were reversible. The ratio of ΔqH+/ΔqO2 induced by thiocyanate varied from 5.0 to 12.0. Current (0.5 to 1.0 ma/cm2) passed through the mucosae, which reversed the normally observed p.d. to values between +70 and +240 mv (secretory side with respect to nutrient side in an external circuit), caused a decrease in qH+ and qO2; the average ΔqH+/ΔqO2 was approximately 13. Using either thiocyanate or electric current the ratio of the induced ΔqH+/ΔqO2 can really exceed 4.0, the electrochemical equivalent of oxygen, and thus if this extra oxygen provides the energy for the extra acid secretion these results invalidate a simple redox pump hypothesis of hydrogen ion transport by gastric mucosa.


1980 ◽  
Vol 239 (6) ◽  
pp. G532-G535 ◽  
Author(s):  
A. Ayalon ◽  
A. Corcia ◽  
G. Klemperer ◽  
S. R. Caplan

The effect of furosemide on acid secretion and Cl- transport was studied in isolated fundic mucosa of the guinea pig. Furosemide (10(-3) M), applied to the serosal side produced an immediate effect on the short-circuit current (Isc), lowering it by 47 +/- 2%. Potential difference decreased by 29 +/- 3%, electrical conductance by 18 +/- 4%, acid secretion by 38 +/- 1%, and net flux of Cl- from serosal-to-mucosal side by 37%. Application of the drug to the mucosal side produced similar effects on acid secretion and on the electrical parameters. It is suggested that furosemide blocks the entrance of Cl-, by the Na+--Cl- cotransport mechanism, through the basolateral membrane of the secreting cell. The consequent reduction in electrogenic Cl- transport would cause Isc and acid secretion to decrease. A reduction of Cl- conductance of the apical membrane, upon mucosal application of the drug, would cause similar effects on acid secretion and Cl- transport.


1991 ◽  
Vol 155 (1) ◽  
pp. 455-467
Author(s):  
R. BRENT THOMSON ◽  
N. AUDSLEY ◽  
JOHN E. PHILLIPS

The commonly used method of passing short-circuit current (Isc) across insect epithelia through Ag-AgCl electrodes, without the use of salt bridges, leads to significant OH− production at the cathode (lumen side) when high currents are applied. The alkalization of the lumen previously reported when cyclic AMP was added to short-circuited locust hindgut is a result of this phenomenon rather than cyclic-AMP-mediated stimulation of acid-base transport in the hindgut. When salt bridges are used to pass short-circuit current across locust hindgut, acid secretion (JH) into the lumen equals alkaline movement (JOH) to the haemocoel side, and JH is similar under both open- and short-circuit conditions. JH is similar (1.5 μequiv cm−2 h−1) in recta and ilea. Addition of cyclic AMP inhibits JH across the rectum by 42–66%, but has no effect on the ileum when salt bridges are used. Electrical parameters (Isc, Vt, Rt) reflecting hindgut Cl− transport (JCL) before and after stimulation with cyclic AMP are the same whether or not salt bridges are used. We found no evidence of any coupling between JCl and JH/JOH.


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