Evidence for a simple Cl− conductance pathway in nutrient membrane of frog stomach

1989 ◽  
Vol 980 (3) ◽  
pp. 367-370 ◽  
Author(s):  
Thomas L. Holloman ◽  
Manuel Schwartz ◽  
Gaspar Carrasquer ◽  
Warren S. Rehm ◽  
Mumtaz A. Dinno
Keyword(s):  
Frog Stomach ◽  
Cl Conductance

Anomalous potential difference responses to changes in sodium concentration in the antrum of frog stomach

1983 ◽  
Vol 245 (4) ◽  
pp. G554-G561 ◽  
Author(s):  
G. Carrasquer ◽  
D. Kissel ◽  
W. S. Rehm ◽  
M. Schwartz
Keyword(s):  
Rana Catesbeiana ◽  
Apical Membrane ◽  
Sodium Concentration ◽  
Potential Difference ◽  
Conductive Pathway ◽  
Luminal Side ◽  
Frog Stomach ◽  
Conductance Ratio ◽  
Cl Conductance

Previously, an electrogenic Na-Cl symport was found in the fundus, and the question arises of whether there is one in the antrum, a tissue that does not secrete acid. In an in vitro preparation of the antrum of Rana catesbeiana, we found that when the [Na+] in nutrient solution was decreased (choline for Na+) the transmucosal potential difference (PD) decreased (the positivity of nutrient side decreased), and when the [Na+] was increased the PD increased. These PD changes were anomalous for Na+ but not for choline. A linear relationship for PD versus log [Na+] and not versus log [choline] excluded a choline conductive pathway. The anomalous PD response was decreased but not abolished by 10(-3) M ouabain. Normal PD responses resulted from [Na+] changes in Cl--free (SO2-4) solutions. PD responses to changes in nutrient [Cl-] were normal but decreased in the absence of Na+. Data are compatible with a passive electrogenic Na-Cl symport with more chloride than sodium ions transported per cycle, as in the fundus. Symport conductance-to-total Cl- conductance ratio is higher in antrum than in the fundus. Data from the luminal side were compatible with apical membrane conductances for Na+ and Cl-.

Further evidence for a simple Cl− conductance pathway in nutrient membrane of frog stomach

1991 ◽  
Vol 1062 (1) ◽  
pp. 113-115 ◽  
Author(s):  
Manuel Schwartz ◽  
Thomas L. Holloman ◽  
Jianyu Zhang ◽  
Gaspar Carrasquer
Keyword(s):  
Frog Stomach ◽  
Cl Conductance

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

scholarly journals Electrophysiological effects of basolateral [Na+] in Necturus gallbladder epithelium.

1992 ◽  
Vol 99 (2) ◽  
pp. 241-262 ◽  
Author(s):  
G A Altenberg ◽  
J S Stoddard ◽  
L Reuss
Keyword(s):  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Resistance ◽  
Membrane Voltage ◽  
Gallbladder Epithelium ◽  
K Channels ◽  
Necturus Gallbladder ◽  
Electrophysiological Effects ◽  
Paracellular Diffusion ◽  
Cl Conductance

In Necturus gallbladder epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.

scholarly journals Ionic events during the volume response of human peripheral blood lymphocytes to hypotonic media. II. Volume- and time-dependent activation and inactivation of ion transport pathways.

1984 ◽  
Vol 83 (4) ◽  
pp. 513-527 ◽  
Author(s):  
B Sarkadi ◽  
E Mack ◽  
A Rothstein
Keyword(s):  
Cell Volume ◽  
Peripheral Blood ◽  
Human Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Time Dependent ◽  
Human Peripheral Blood Lymphocytes ◽  
Cl Transport ◽  
Anion Conductance ◽  
Volume Response ◽  
Cl Conductance

Hypotonic dilution of human peripheral blood lymphocytes (PBL) induces large conductive permeabilities for K+ and Cl-, associated with the capacity of the cells to regulate their volumes. When rapid cation leakage is assured by the addition of the ionophore gramicidin, the behavior of the anion conductance pathway can be independently examined. Using this technique it is demonstrated that the volume-induced activation of Cl- transport is triggered at a threshold of approximately 1.15 X isotonic cell volume. If the volume of a cell is increased to this level or above, the Cl- transport system is activated, whereas if the volume of a swollen cell is decreased below the threshold value, the Cl- transport is inactivated. Activation and inactivation are independent of the relative volume changes and of the actual cellular Na+, K+, or Cl- concentrations, as well as of the changes in membrane potential in PBL. When net salt movement and thus volume change are inhibited by specific blockers of K+ transport (e.g., quinine, or Ca2+ depletion), volume-induced Cl- conductance shows a time-dependent inactivation, with a half-time of 5-8 min. The Cl- conductance, when activated, appears to involve an all-or-none response. In contrast, volume-induced K+ conductance is a graded response, with the increase in K+ flux being roughly proportional to the hypotonicity-induced increase in cell volume. The data indicate that during lymphocyte volume response in hypotonic media, anion conductance increases by orders of magnitude, exceeding the K+ conductance, so that the rate of the volume decrease (KCl efflux) is determined by a graded alteration in K+ conductance. When the cell volume approaches the isotonic value, it is stabilized by the inactivation of the anion conductance pathway.

Active NaCl absorption across split lamellae of posterior gills of the chinese crab Eriocheir sinensis: stimulation by eyestalk extract

2000 ◽  
Vol 203 (8) ◽  
pp. 1373-1381 ◽  
Author(s):  
H. Onken ◽  
A. Schobel ◽  
J. Kraft ◽  
M. Putzenlechner
Keyword(s):  
Electromotive Force ◽  
Single Channel ◽  
Short Circuit ◽  
Noise Analysis ◽  
Eriocheir Sinensis ◽  
Dialysis Tubing ◽  
Channel Current ◽  
Dose Dependent ◽  
Cl Conductance ◽  
Stimulation Of

Split lamellae of the posterior gills of freshwater-adapted Chinese crabs (Eriocheir sinensis) were mounted in a modified Ussing-type chamber, and active and electrogenic absorption of Na(+) and Cl(−) were measured as positive (I(Na)) or negative (I(Cl)) short-circuit currents. Haemolymph-side addition of eyestalk extract stimulated I(Cl) by increasing both the transcellular Cl(−) conductance and the electromotive force for Cl(−) absorption. The effect was dose-dependent. Boiling the eyestalk extract did not change its effectiveness. The stimulating factor passed through dialysis tubing, indicating that it has a molecular mass of less than 2 kDa. R(p)cAMPS, a blocker of protein kinase A, reduced the stimulated I(Cl). Eyestalk extract stimulated I(Na) by increasing the transcellular Na(+) conductance at constant electromotive force. Amiloride-induced current-noise analysis revealed that stimulation of I(Na) was accompanied by an increase in the apparent number of open apical Na(+) channels at a slightly reduced single-channel current. In addition to the electrophysiological experiments, whole gills were perfused in the presence and in the absence of putative transport stimulators, and the specific activities of the V-ATPase and the Na(+)/K(+)-ATPase were measured. Eyestalk extract, theophylline or dibutyryl-cyclic AMP stimulated the activity of the V-ATPase, whereas the activity of the Na(+)/K(+)-ATPase was unaffected. The simultaneous presence of R(p)cAMPS prevented the stimulation of V-ATPase by eyestalk extract or theophylline.

Helicobacter pyloricytotoxin VacA increases alkaline secretion in gastric epithelial cells

2001 ◽  
Vol 281 (6) ◽  
pp. G1440-G1448 ◽  
Author(s):  
Lucantonio Debellis ◽  
Emanuele Papini ◽  
Rosa Caroppo ◽  
Cesare Montecucco ◽  
Silvana Curci
Keyword(s):  
Apical Membrane ◽  
Acid Output ◽  
Human Infection ◽  
Gastric Epithelium ◽  
Secondary Development ◽  
Acute Effects ◽  
Gastric Diseases ◽  
Gastric Glands ◽  
Frog Stomach ◽  
Alkaline Secretion

Human infection by the bacterium Helicobacter pylori (Hp) may lead to severe gastric diseases by an ill-understood process involving several virulence factors. Among these, the cytotoxin VacA is associated with higher tissue damage. In this study, the isolated frog stomach model was used to characterize the acute effects of VacA on the gastric epithelium. Our results show that VacA partially inhibits gastric acid output by increasing HCO[Formula: see text] efflux. Experiments conducted with double-barrelled pH or Cl−-selective microelectrodes on surface epithelial gastric cells (SECs) and single gastric glands show that VacA does not impair the activity of the oxyntic cells but renders the apical membrane of SECs more permeable to HCO[Formula: see text] and Cl−. Inhibition of this permeation by 5-nitro-2-(3-phenylpropylamino) benzoic acid indicates that this may be due to the formation of anion-selective pores by the toxin. We suggest that VacA-dependent HCO[Formula: see text] efflux from SECs improves the environmental conditions (pH, CO2concentration) of the niche parasitized by Hp, that is the gastric surface. This may favor Hp persistence in the tissue and the secondary development of a chronic inflammation.

Activation of CFTR Cl- conductance in polarized T84 cells by luminal extracellular ATP

1995 ◽  
Vol 268 (2) ◽  
pp. C425-C433 ◽  
Author(s):  
M. J. Stutts ◽  
E. R. Lazarowski ◽  
A. M. Paradiso ◽  
R. C. Boucher
Keyword(s):  
Adenosine Receptor ◽  
Apical Membrane ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Apical Cell ◽  
Extracellular Atp ◽  
T84 Cells ◽  
Apical Cell Membrane ◽  
Cl Secretion ◽  
Cl Conductance

Luminal extracellular ATP evoked a bumetanide-sensitive short-circuit current in cultured T84 cell epithelia (90.2 +/- 18.2 microA/cm2 at 100 microM ATP, apparent 50% effective concentration, 11.5 microM). ATP appeared to increase the Cl- conductance of the apical membrane but not the driving force for Cl- secretion determined by basolateral membrane K+ conductance. Specifically, the magnitude of Cl- secretion stimulated by ATP was independent of basal current, and forskolin pretreatment abolished subsequent stimulation of Cl- secretion by ATP. Whereas ATP stimulated modest production of adenosine 3',5'-cyclic monophosphate (cAMP) by T84 cells, ATP caused smaller increases in intracellular Ca2+ and inositol phosphate activities than the Ca(2+)-signaling Cl- secretagogue carbachol. An inhibitor of 5'-nucleotidase, alpha,beta-methyleneadenosine 5'-diphosphate, blocked most of the response to luminal ATP. The adenosine receptor antagonist 8-(p-sulfophenyl)theophylline blocked both the luminal ATP-dependent generation of cAMP and Cl- secretion when administered to the luminal but not submucosal bath. These results demonstrate that the Cl- secretion stimulated by luminal ATP is mediated by a A2-adenosine receptor located on the apical cell membrane. Thus metabolism of extracellular ATP to adenosine regulates the activity of cystic fibrosis transmembrane conductor regulator (CFTR) in the apical membrane of polarized T84 cells.

scholarly journals Interaction between the Cl ‐ conductance associated proteins bestrophins and TMEM16A? (1077.2)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Christian Aalkjaer ◽  
Vibeke Dam ◽  
Donna Boedtkjer ◽  
Vladimir Matchkov
Keyword(s):  
Associated Proteins ◽  
Cl Conductance
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