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.

Ba2+ inhibition of electrogenic Cl- secretion in vitro frog and piglet gastric mucosa

1980 ◽  
Vol 239 (3) ◽  
pp. G151-G160 ◽  
Author(s):  
W. L. McLennan ◽  
T. E. Machen ◽  
T. Zeuthen
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Surface Charges ◽  
Inhibitory Effects ◽  
Cl Secretion ◽  
High K ◽  
In Vitro Investigation ◽  
Newborn Pigs

Gastric mucosae from frogs and newborn pigs were used for in vitro investigation of the effects of Ba2+ (10 microM to 7 mM) on transepithelial potential difference (PD), resistance and conductance (G), short-circuit current (Isc), H+ secretion, and transepithelial fluxes of 36Cl-. Ba2+ in the serosal, but not the mucosal, solution of both preparations caused PD, G, Isc, and Cl- secretion (JnetCl, Isc conditions) to decrease, while H+ secretion remained constant. Because the oxyntic cells were most likely the site of action for Ba2+, these cells must have the capacity to secrete Cl- in excess of H+ ions. The inhibitory effect of Ba2+ was not due to competition in the serosal membrane by Ba2+ for surface charges, Ca2+ sites, Na+ sites, or Cl- sites. When [K+] in both the mucosal and serosal solutions or in just the serosal solution ([K+]s) alone was increased to 10 mM, the inhibitory effects of low [Ba2+] were reduced; however, at higher [Ba2+], Isc was stimulated. At least part of the Ba2+ effect seems to be due to blockage of K+ channels in the serosal membrane of oxyntic cells. High [K+]s also caused decreased PD and Isc (but increased G) with no change in H+ secretion. It is proposed that during Isc conditions, JnetCl involves a neutral Na+-dependent accumulation of Cl- within oxyntic cells and a passive, conductive efflux fromthe cells into the mucosal solution. Ba2+ and high [K+] may alter this transport by depolarizing and, under certain conditions, hyperpolarizing intracellular voltage.

Water and electrolyte transport by rabbit esophagus

1975 ◽  
Vol 229 (2) ◽  
pp. 438-443 ◽  
Author(s):  
DW Powell ◽  
SM Morris ◽  
DD Boyd
Keyword(s):  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Potential Difference ◽  
Sodium Absorption ◽  
Bathing Solution ◽  
Electrical Potential Difference

The nature of the transmural electrical potential difference and the characteristics of water and electrolyte transport by rabbit esophagus were determined with in vivo and in vitro studies. The potential difference of the perfused esophagus in vivo was -28 +/- 3 mV (lumen negative). In vitro the potential difference was -17.9 +/- 0.6 mV, the short-circuit current 12.9 +/- 0.6 muA/cm2, and the resistance 1,466 +/- 43 ohm-cm2. Net mucosal-to-serosal sodium transport from Ringer solution in the short-circuited esophagus in vitro accounted for 77% of the simultaneously measured short-circuit current and net serosal-to-mucosal chloride transport for 14%. Studies with bicarbonate-free, chloride-free, and bicarbonate-chloride-free solutions suggested that the net serosal-to mucosal transport of these two anions accounts for the short-circuit current not due to sodium absorption. The potential difference and short-circuit current were saturating functions of bathing solution sodium concentration and were inhibited by serosal ouabain and by amiloride. Thus active mucosal-to-serosal sodium transport is the major determinant of the potential difference and short-circuit current in this epithelium.

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.

Sodium transport by lamb proximal colon measured during early postnatal development

1982 ◽  
Vol 98 (1) ◽  
pp. 155-159 ◽  
Author(s):  
M. W. Smith ◽  
P. S. James
Keyword(s):  
Postnatal Development ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Early Postnatal Development ◽  
The Third ◽  
Electrolyte Absorption ◽  
Chloride Absorption

SUMMARYProximal colons taken from lambs up to 3 weeks after birth were shown to transport both sodium and chloride from lumen to blood when incubated in vitro.Sodium transport fell into three phases during postnatal development. The first covered the period from birth to 3 days of age when sodium transport was high and equal to that calculated from measurement of short-circuit current. The second was seen in 5- and 7-day-old lambs where the short-circuit current was low and the net transport of sodium was negligible. The third was seen in 2-3-week-old lambs where sodium transport was high, but the short-circuit current was low.Chloride absorption by colons taken from 1-day-old lambs appeared to be in exchange for an anion, possibly bicarbonate. Chloride absorption by colons taken from 3-week-old lambs appeared to be electrogenie or coupled directly to the transport of sodium.A possible explanation for the failure of electrolyte absorption by colons taken from 5- and 7-day-old lambs is discussed.

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(-).

Modulation of aldosterone-induced stimulation of ENaC synthesis by changing the rate of apical Na+ entry

2001 ◽  
Vol 281 (4) ◽  
pp. F687-F692 ◽  
Author(s):  
Lisette Dijkink ◽  
Anita Hartog ◽  
Carel H. Van Os ◽  
René J. M. Bindels
Keyword(s):  
Feedback Inhibition ◽  
Collecting Duct ◽  
Short Circuit ◽  
Primary Cultures ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Cortical Collecting Duct ◽  
Entry Rate ◽  
Protein Levels ◽  
Stimulation Of

Primary cultures of immunodissected rabbit connecting tubule and cortical collecting duct cells were used to investigate the effect of apical Na+ entry rate on aldosterone-induced transepithelial Na+ transport, which was measured as benzamil-sensitive short-circuit current ( I sc). Stimulation of the apical Na+ entry, by long-term short-circuiting of the monolayers, suppressed the aldosterone-stimulated benzamil-sensitive I sc from 320 ± 49 to 117 ± 14%, whereas in the presence of benzamil this inhibitory effect was not observed (335 ± 74%). Immunoprecipitation of [35S]methionine-labeled β-rabbit epithelial Na+ channel (rbENaC) revealed that the effects of modulation of apical Na+ entry on transepithelial Na+ transport are exactly mirrored by β-rbENaC protein levels, because short-circuiting the monolayers decreased aldosterone-induced β-rbENaC protein synthesis from 310 ± 51 to 56 ± 17%. Exposure to benzamil doubled the β-rbENaC protein level to 281 ± 68% in control cells but had no significant effect on aldosterone-stimulated β-rbENaC levels (282 ± 68%). In conclusion, stimulation of apical Na+ entry suppresses the aldosterone-induced increase in transepithelial Na+transport. This negative-feedback inhibition is reflected in a decrease in β-rbENaC synthesis or in an increase in β-rbENaC degradation.

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+].

Measurement of short-circuit current and ion transport across the ileum

1964 ◽  
Vol 206 (3) ◽  
pp. 658-668 ◽  
Author(s):  
T. W. Clarkson ◽  
S. R. Toole
Keyword(s):  
Ion Transport ◽  
Sodium Transport ◽  
Chemical Potential ◽  
Short Circuit ◽  
Silver Ions ◽  
Short Circuit Current ◽  
Chloride Ions ◽  
Salt Transport ◽  
Complexing Agents ◽  
Bathing Solution

An apparatus is described which allowed control over both the electrical and chemical potential gradients across the isolated ileum of the rat and at the same time permitted the measurement of the transport of ions and water. Silver ions, released from the electrodes, affected ion transport. In the absence of complexing agents, the short-circuit current ( SCC) fell during the 60-min measurement period and was equal to the net sodium transport. With 10–3 m reduced glutathione in the bathing solution, the SCC was constant and equal to 94% of the sodium transport. With 10–4 m cysteine, the SCC was greatly increased. Sodium transport, also increased, was equal to 75% and chloride secretion to 20% of the SCC. A mechanism by which silver ions stimulate sodium transport, is proposed. Comparison of water and salt transport between open- and short-circuited tissues indicated that chloride ions were more effective in producing water movement when transported from mucosal to serosal solutions directly through the tissue (open circuit) rather than via the Ag/AgCl electrode system (short-circuit experiments).

Intestinal mucosal cyclic GMP: regulation and relation to ion transport

1976 ◽  
Vol 231 (1) ◽  
pp. 275-282 ◽  
Author(s):  
TA Brasitus ◽  
M Field ◽  
DV Kimberg
Keyword(s):  
Causal Relationship ◽  
Cyclic Gmp ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ileal Mucosa ◽  
Muscarinic Cholinergic Receptors ◽  
Cholecystokinin Octapeptide ◽  
Muscarinic Cholinergic ◽  
Stimulation Of

Stimulation of alpha-adrenergic and muscarinic cholinergic receptors in rabbit ileal mucosa in vitro produced 5- to 15-fold increases in cyclic GMP (cGMP) concentration that were maximal within 2 min and gone within 30 min. Cholecystokinin octapeptide and insulin caused similar increases in cGMP. None of these agents affected cAMP. The epinephrine-induced increase in cGMP was blocked by atropine at 100 but not at 1 muM concentration. Epinephrine stimulates active NaCl absorption and decreases short-circuit current (SCC) in vitro, the latter effect due to inhibition of HCO3 secretion. Atropine (100 muM) blocked the former but not the latter effect of epinephrine. In vitro additions of several concentrations of cGMP and 8-bromo-cGMP did not decrease SCC or alter Na fluxes. Thus, changes in cGMP concentration have been directly correlated with changes in active absorption of NaCl, but a causal relationship has not been proven.

Response of active transport of ions and spontaneous water flux to osmotic gradients in gastric mucosa

1975 ◽  
Vol 228 (3) ◽  
pp. 738-741 ◽  
Author(s):  
L Villegas
Keyword(s):  
Gastric Mucosa ◽  
Water Content ◽  
Water Movement ◽  
Short Circuit ◽  
Water Flux ◽  
Short Circuit Current ◽  
Ion Flux ◽  
Bathing Solution ◽  
Cell Water ◽  
Concentration Gradients

The effects of symmetric changes of the mucosal and serosal bathing solution on cell water content, net ion flux, and net water movement were studied in the isolated frog gastric mucosa. Similar to transmucosal concentration gradients that induce water movement and changes in cell water content, symmetric osmolality changes of the bathing solutions also produce changes in these functional parameters. Thus, increments from 165 to 286 mosmol/kg water in the osmolality of both solutions reduce cell water content from 2.37 plus or minus 0.12 to 1.30 plus or minus 0.20 ml/g wt, the net ion flux (acid secretion plus short-circuit current) from 4.83 plus or minus 0.36 to 3.44 plus or minus 0.26 mueq/cm2 per h, and the net water flux from 10.6 plus or minus 1.1 to 2.4 plus or minus 1.2 mul/cm2 per h. These osmotically induced flux changes of water and ions must be considered when osmotic gradients are being used to generate and to evaluate water movement across the gastric mucosa.

Sign in / Sign up

Export Citation Format

Share Document