PARASYMPATHETIC ACTION ON GASTRIC BIOELECTRIC POTENTIAL IN RATS

1967 ◽  
Vol 45 (2) ◽  
pp. 281-290 ◽  
Author(s):  
H. Allan Ridley ◽  
Burton E. Vaughan ◽  
Joseph T. Cummins
Keyword(s):  
Acid Secretion ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Detectable Effect ◽  
Partial Recovery ◽  
Bioelectric Potential ◽  
Rat Stomach ◽  
Solution Bathing ◽  
Isolated Rat

The gastric bioelectric potential in vitro was consistently lower in stunned rats than in rats anesthetized with ether, or decapitated. This depressed potential was prevented by vagotomy and by atropine either subcutaneously injected or directly instilled. Similarly, transmural potential and short-circuit current were sharply reduced, by one-half, when the solution bathing the mucosal surface was made 10−2 M in acetylcholine (ACh). There was no detectable effect on transmural conductance (dI/dE). Inhibition of potential was proportional to ACh concentration from 10−5 M to 10−2 M. Partial recovery was demonstrated by rinsing and replacing solutions; atropine at 10−4 M irreversibly blocked such inhibition. Tubocurarine at 10−3 M did not change the response, when added prior to ACh, while physostigmine at 10−4 M enhanced the effect of ACh. The ACh analogues acetyl-β-methylcholine, acetylthiocholine, and carbamylcholine, at 10−3 M, reduced potential, as did ACh at 10−3 M. Carbamylcholine, which is not appreciably hydrolyzed by acetylcholinesterase, showed only slightly greater effect than ACh. In these studies, bioelectric potential was altered without any change in the acid secretion rate. This supports other studies demonstrating independence in the isolated rat stomach of electrical and acid secretion parameters.

Ba++ on the resting frog stomach: effects on electrical and secretory parameters

1975 ◽  
Vol 228 (2) ◽  
pp. 511-517 ◽  
Author(s):  
PK Rangachari
Keyword(s):  
Acid Secretion ◽  
Nutrient Solution ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Secretory Rate ◽  
Frog Stomach ◽  
Solution Bathing ◽  
Per Se

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.

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.

Acid secretion in fetal rat stomach in vitro

1981 ◽  
Vol 240 (3) ◽  
pp. G206-G210
Author(s):  
R. Ducroc ◽  
J. F. Desjeux ◽  
B. Garzon ◽  
J. P. Onolfo ◽  
J. P. Geloso
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Rat Stomach ◽  
Passive Permeability ◽  
Anion Secretion ◽  
Ussing Chambers ◽  
Ionic Fluxes ◽  
Fetal Rat

In vivo fetal rat stomach produces HCl 48 h before birth. This study examines the mechanisms of H+ secretion from days 19 to 21 before birth. Isolated fetal stomachs were mounted as flat sheets in Ussing chambers for measurement of the transepithelial H+ fluxes (JH+) and short-circuit current (Isc), as indexes of the active ionic fluxes, and for measurement of total ionic conductance (G) and unidirectional mannitol fluxes from serosa to mucosa (JMans leads to m), as indexes of passive permeability. The results indicate that JH+ was absent at day 19 but reached 0.75 +/- 0.1 and 0.75 +/- 0.09 mueq . h-1 . cm-2 at days 20 and 21, respectively. Concomitantly, Isc increased significantly (56%) between days 19 and 20 in the direction of anion secretion or cation absorption. Parallel reductions in G (45%) and in JMans leads to m (66%) were observed between days 19 and 20. In conclusion, the simultaneous appearance of active H+ secretion and decreased passive transepithelial permeability strongly suggests that both processes are involved in the mechanism of acidification of the fetal rat stomach before birth.

Adrenergic agents stimulate and cholinergic agents inhibit H+ secretion by amphibian jejunum

1986 ◽  
Vol 251 (3) ◽  
pp. G405-G412
Author(s):  
J. F. White ◽  
R. Britanisky
Keyword(s):  
Acid Secretion ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Atpase Inhibitor ◽  
Adrenergic Agents ◽  
Cholinergic Agents ◽  
Ph Stat ◽  
Opposing Effects ◽  
Dose Dependent Increase

In vitro segments of Amphiuma jejunum secrete H+ spontaneously. This study explored the effect of cholinergic and adrenergic agents on H+ secretion. Segments of mucosa were short-circuited and exposed on their mucosal surface to HCO3- -buffered medium while the pH of the unbuffered serosal medium was held by the pH-stat technique. Methacholine added to the serosal medium nearly abolished the spontaneous short-circuit current (Isc) and serosal alkalinization (JHCO3-) with an EC50 of 3.7 X 10(-7) M. Subsequent addition of norepinephrine (NE) to the serosal medium caused a dose-dependent increase in Isc and JHCO3. For three catecholamines the order of potency was epinephrine greater than NE greater than isoproterenol. The spontaneous Isc was significantly reduced (P less than 0.05) by the gastric H+-K+-ATPase inhibitor omeprazole, while the NE-induced Isc was unaltered by the inhibitor. Replacement of medium Na+ with choline abolished the response to NE. The NE-induced Isc was also reduced by methacholine. Acetazolamide inhibited the spontaneous and NE-induced Isc and JHCO3. In summary, cholinergic and adrenergic agents have opposing effects on intestinal H+-HCO3- transport. Jejunal acid secretion may be controlled in part by these antagonistic influences. Adrenergically activated acid secretion occurs by a different mechanism than spontaneous acid secretion.

scholarly journals Ion Transport in Isolated Rabbit Ileum

1964 ◽  
Vol 47 (6) ◽  
pp. 1043-1059 ◽  
Author(s):  
Stanley G. Schultz ◽  
Ralph Zalusky
Keyword(s):  
Short Circuit ◽  
Sugar Transport ◽  
Short Circuit Current ◽  
Metabolic Fate ◽  
Na Transport ◽  
Perfusion Medium ◽  
Rabbit Ileum ◽  
Low Concentrations ◽  
Solution Bathing

The addition of actively transported sugars to the solution bathing the mucosal surface of an in vitro preparation of distal rabbit ileum results in a rapid increase in the transmural potential difference, the short-circuit current, and the rate of active Na transport from mucosa to serosa. These effects are dependent upon the active transport of the sugar per se and are independent of the metabolic fate of the transported sugar. Furthermore, they are inhibited both by low concentrations of phlorizin in the mucosal solution and by low concentrations of ouabain in the serosal solution. The increase in the short-circuit current, ΔIsc, requires the presence of Na in the perfusion medium and its magnitude is a linear function of the Na concentration. On the other hand, ΔIsc is a saturable function of the mucosal sugar concentration which is consistent with Michaelis-Menten kinetics suggesting that the increase in active Na transport is stoichiometrically related to the rate of active sugar transport. An interpretation of these findings in terms of a hypothetical model for intestinal Na and sugar transport is presented.

Acid secretion, potential difference, and resistance of elasmobranch stomach

1962 ◽  
Vol 203 (6) ◽  
pp. 1091-1093 ◽  
Author(s):  
Warren S. Rehm
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Present Report ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Potential Difference ◽  
Secretory Rate ◽  
Negaprion Brevirostris ◽  
Ion Secretion

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.

Effects of amphotericin B on ionic transport and sodium permeability of the toad lens

1975 ◽  
Vol 229 (6) ◽  
pp. 1520-1525 ◽  
Author(s):  
PJ Bentley ◽  
OA Candia
Keyword(s):  
Amphotericin B ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Anterior Surface ◽  
Sodium Permeability ◽  
Solution Bathing ◽  
Net Flux ◽  
Large Decline

The polyene antibiotic amphotericin B decreases the PD and short-circuit current (SCC) across the amphibian lens in vitro. It was only effective when placed in the solution at the anterior side and its effect was reversible. Amphotericin B caused a large decline in the PD across the anterior surface of the lens and a smaller reduction in the PD across the posterior side. This seems to be due to a direct decrease of the electrical resistance of the anterior face. The effects required the presence of sodium in the Ringer solution bathing the anterior surface. The translenticular Na fluxes were increased in both directions so that the net flux changed little. Amphotericin B produced a considerable increase in the rate of accumulation of sodium and loss of potassium by the lens. The oxygen consumption of the lens was unchanged by amphotericin B. Amphotericin B appears to act on the lens epithelium by selectively increasing its passive sodium permeability.

OSMOTIC INHIBITION OF THE NATRIFERIC RESPONSE OF THE TOAD URINARY BLADDER TO VASOPRESSIN

1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY
Keyword(s):  
Urinary Bladder ◽  
Water Movement ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Electrical Potential Difference ◽  
Osmotic Gradient

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.

Protein kinase C potentiates cAMP-stimulated mouse duodenal mucosal bicarbonate secretion in vitro

2004 ◽  
Vol 286 (5) ◽  
pp. G814-G821 ◽  
Author(s):  
Bi-Guang Tuo ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett ◽  
Jon I. Isenberg
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Duodenal Mucosa ◽  
Bicarbonate Secretion ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ussing Chambers ◽  
Duodenal Bicarbonate Secretion

PKC has been shown to regulate epithelial Cl- secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current ( Isc). When PMA and dibutyryl-cAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc ( P > 0.05). However, a 1-h preincubation with PMA potentiated db-cAMP-stimulated duodenal bicarbonate secretion and Isc in a concentration-dependent manner (from 10-8 to 10-5M) ( P < 0.05). PMA preincubation had no effects on carbachol- or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKCα, -γ, -ϵ, -θ, -μ, and -ι/λ were expressed in murine duodenal mucosa. Ro 31–8220 (an inhibitor active against PKCϵ, -α, -β, and -γ), but not Gö 6983 (an inhibitor active against PKCα, -γ, -β, and -δ), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time- and concentration-dependently increased the activity of PKCϵ, an effect that was prevented by Ro 31–8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKCϵ isoform.

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