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S Curci

Publications and source records attributed to S Curci.

At least 37 records · Page 2Linked to original sources
PubMed1987

Evidence for rheogenic sodium bicarbonate cotransport in the basolateral membrane of oxyntic cells of frog gastric fundus.

Ionic conductance properties of the basolateral cell membrane of oxyntic cells were studied in frog gastric fundus in vitro. After mounting the fundus in a modified Ussing chamber the serosal connective tissue was dissected off and individual oxyntic cells were punctured from the serosal surface with microelectrodes. Under resting conditions the membrane potential averaged -56.9, SD +/- 9.5 mV (n = 63), cytoplasm negative. Lowering or raising serosal HCO-3 concentration from 17.8 to 6 or 36 mmol/l respectively at constant PCO2 depolarized or hyperpolarized the cell membrane by +16.7 or -18.2 mV respectively. Sudden removal of serosal Na+ also depolarized the cell membrane (anomalous Nernst response). Since both the HCO-3 dependent and the Na+ dependent potential changes were strongly depressed by the disulfonic stilbene SITS and since the potential response to HCO-3 was virtually abolished in Na+-free solution we conclude that a rheogenic Na+ (HCO-3)n-cotransport system (n greater than 1) is present in the basolateral cell membrane of oxyntic cells. Its possible role in base transfer during HCl-secretion or HCO-3 secretion remains to be elucidated.

Animals↗
PubMed1986

Histamine reduces Cl- activity in surface epithelial cells of frog gastric mucosa. Suggestive evidence for ionic coupling between surface epithelial and oxyntic cells.

Intracellular chloride activity (acCl) and serosal as well as mucosal membrane potentials (Vcs and Vcm) were recorded in surface epithelial cells (SEC) of frog gastric mucosa during the resting state (cimetidine, 10(-4) mol/l) or during stimulation with histamine (10(-4) mol/l). Stimulation leads to a fall in acCl from 18.7 SD +/- 5.9 mmol/l (n = 26) to 13.3 SD +/- 4.9 mmol/l (n = 33). Simultaneously both cell membranes hyperpolarize, Vcs from -56.0 SD +/- 4.8 (n = 42) to -62.8 +/- 7.6 (n = 43) and Vcm from -39.6 SD +/- 5.8 (n = 42) to -47.9 +/- 7.6 (n = 43), so that intracellular chloride remains elevated above electrochemical equilibrium at both cell membranes. Reduction or omission of chloride in the lumen perfusate does not affect acCl, suggesting that the luminal cell membrane is virtually tight for chloride ions. Current induced hyperpolarization of the serosal cell membrane potential which simulates the electrical effects of stimulation, does not affect acCl either; however, inhibition of gastric acid secretion by a benzimidazol derivative which is known to block the H+/K+ ATPase prevents the fall in acCl in response to histamine. The same holds if the experimental solutions are gassed with 25% CO2 which does not interfere with acid secretion but may block cell to cell communication via gap junctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

On the luminal membrane permeability to Cl- of necturus gastric surface cells.

The surface cells (SEC) luminal membrane conductance to Cl- was tested on the resting Necturus gastric mucosa by applying conventional and Cl--sensitive microelectrodes under luminal low-Cl- conditions. Reduction of chloride (2 mmol/1) in the luminal bath did not result in any detectable reduction of intracellular Cl-. Therefore, in analogy to previous findings on the frog SEC, also the luminal membrane of the Necturus surface cells appears to have a negligible conductance to Cl-. The data speak against a relevant role of the amphibian SEC in the non-acidic Cl- secretion.

Animals↗
PubMed1984

[Intracellular activity of Cl- measured with microelectrodes selective for Cl- in superficial epithelial cells of gastric mucosa at "rest"].

Intracellular chloride activity and the electrical membrane potential differences were determined in surface epithelial cells of frog fundic gastric mucosa in resting conditions. Separate measurements were carried out by applying single barreled, (KCl filled), conventional and liquid Cl- -selective microelectrodes. Membrane potentials with respect to the serosal (psi cs) and mucosal surfaces (psi cm) recorded with conventional microelectrodes, were -67 +/- E.S. 1.7 mV and -39.9 mV (as calculated from psi cs and psi T) respectively. The average electrical potential measured with Cl- -selective microelectrodes with respect to the serosal bath (psi Cl-cs) was -30.5 +/- E.S. 1.9 mV which yields an intracellular Cl- activity of 14 mmol/l, a value that is 2.8 times that predicted for an equilibrium distribution across the serosal membrane. On the contrary, Cl- seems to be distributed at equilibrium across the mucosal membrane. These results indicate that Cl- is accumulated across the serosal membrane into gastric cells in an energy requiring step.

Animals↗
PubMed1984

Effect of external sodium on intracellular chloride activity in the surface cells of frog gastric mucosa. Microelectrode studies.

The intracellular chloride activity and its dependence on ionic substitutions in the bathing media was studied in individual surface cells of resting gastric mucosa using conventional and Cl- selective microelectrodes. When the tissue was perfused with control NaCl-Ringer the cell membrane p.d.'s, cell-lumen (psi cm) and cell-serosa (psi cs) were -40.9 +/- 0.6 mV and -66.8 +/- 0.5 mV (n = 175) respectively and the p.d. measured by the Cl- selective microelectrodes across the serosal membrane (psi csCl-) averaged -32.4 +/- 0.7 mV (n = 138). From these values an intracellular Cl- activity (acCl-) of 15.3 mmol/l can be estimated. The data indicate that chloride ion is distributed close to equilibrium at the luminal membrane while it is accumulated by an energy requiring step at the serosal membrane. Reduction (2 mmol/l) or absence of chloride from the luminal bath did not result in any detectable change of acCl-; on the other hand, after removal of Cl- from the serosal bath the intracellular Cl- activity fell to 7.1 mmol/l. When the tissue was exposed to serosal Na+-free Ringer (Na+ replaced by choline or TMA), although the acCl- remained unaffected, a marked reduction of the electrochemical gradient for Cl- at the serosal membrane was observed. These data indicate that: chloride is accumulated in the surface cells against its electrochemical potential difference at the serosal membrane; the luminal membrane has a negligible conductance to Cl-, while the serosal membrane represents a conductive pathway to chloride; the uphill entry of chloride at the serosal membrane seems to be, at least partially, Na+-dependent.

Animals↗
PubMed1983

[Effect of ionophore A23187 on the response to ADH in the ventral skin of Rana esculenta].

The addition of the Ca++ ionophore A23187 (10 microM) to the inside solution of the frog skin induced a transient increase in the active Na+ transport in frog skin (Rana esculenta) which decayed to the control values 60 minutes after the addition. At the same time the skin resistance failed significantly; antidiuretic hormone addition resulted in no-more increase of the Na+ active transport; the skin resistance remained unchanged. To further investigate the role of intracellular calcium on the skin transepithelial permeability, the effect of A23187 ionophore on thiourea permeability has been tested. Increase in intracellular Ca++ concentration brought about by calcium ionophores have been shown to modify both basal and ADH-stimulated thiourea transport.

Animals↗
PubMed1983

[Effect of niflumic acid on the non-acid transport of chlorides in the gastric mucosa of amphibians].

The in vivo gastric mucosa actively transport Cl- (serosa to mucosa) and it has been shown that the e.m.f. generated by the epithelium, as well as the short circuit current are both manifestations of the same phenomenon: the Cl- movement. Also, it has been postulated the presence of a Cl- - HCO-3 exchange in the gastric epithelium probably located on different cell types. The addition of niflumic acid (10(-4) M in the serosal solution) resulted in a decline towards zero of both transepithelial p.d. and Isc. The mechanism of the niflumic acid action is postulated to be a blockage of the Cl- - HCO-3 exchange, similarly to the SITS action mechanism.

Animals↗
PubMed1980

Intracellular potassium activity in epithelial cells of frog fundic gastric mucosa.

Microelectrodes were used to measure membrane potential and intracellular potassium activity in surface epithelial cells (SEC) of frog (Rana esculenta) fundic gastric mucosa in vitro. Separate measurements were carried out by applying fine-tipped, single barrelled, KCl filled non-selective electrodes and liquid K+ -selective electrodes. Membrane potentials with respect to the mucosal and serosal surfaces, measured with non-selective electrodes, were -54.5 +/- 1.0 S.E mV (n = 59) and -73.0 +/- 1.1 S.E. mV (n = 59) respectively. The electrical potential difference referred to the mucosal surface, when measured with K+ -sensitive electrodes, was +21.2 +/- 0.8 S.E mV (n = 35), and intracellular K+ activity was 98.5 mmol/l. Assuming that intracellular and extracellular K+ activity coefficients are equal (gamma K = gamma K), the K+ concentration is 135.0 mmol/l. The K+ equilibrium potential, EK, was calculated as -90. mV i.e. more negative than both membrane potentials. This result indicates active potassium accumulation in the SEC and provides direct evidence of the presence of an active K+ pump in either both or in only one of the cell membranes.

Animals↗
PubMed1980

Effect of cycloheximide on urea facilitated transport through toad gallbladder epithelium.

Transepithelial urea outfluxes across toad gallbladder were determined before and after the addition of cycloheximide. The drug inhibits the movement of urea but has no effect on thiourea and antipyrine outfluxes. The inhibition of amide transport is time dependent as also shown in counterflow experiments. These results are consistent with the hypothesis that cycloheximide inhibits the synthesis of membrane proteic sites involved in urea mediated transport.

Animals↗
PubMed1978

Facilitated transport of urea across the gall-bladder luminal membrane.

Counterflow experiments demonstrate the existence of urea counter-transport on the epithelium luminal surface. This phenomenon disappears when 10(-4) M phloretin is added to the perfusion fluid. Moreover counterflow experiments made using thiourea as elicitor, demonstrate that the phenomenon is specific for the urea.

Animals↗
PubMed1976

Facilitated transport of urea across the toad gallbladder.

The toad gallbladder epithelium is much more selective than that of the rabbit especially as to the permeability of two molecules like urea and thiourea. These observations can probably be attributed to different permeation mechanisms of the 2 molecules. Neither active transport nor solvent drag can explain these phenomena. 10(-4) M phloretin strongly inhibits urea movement, but does not alter either thiourea fluxes or isotonic net water transport: these results suggest that a specific mechanism is involved in urea movement. The urea transport shows saturation kinetic which is consistent with the presence of a facilitated mechanism.

Animals↗
PubMed1975

Permeability pathways for non-electrolytes through Bufo bufo gall-bladder.

Amphotericin B treatment increases the thiourea, D-xylose and mannitol fluxes and lowers those of urea, N-methyl-urea, acetamide, formamide, and N-N'-dimethyl-thiourea. The degree of flux inhibition is related to the cellular permeability of these compounds. Most probably Amphotericin B increases the permeability of all those molecules across the luminal plasma membrane, but simultaneously elicits a cellular swelling, which reduces the diffusion across the lateral plasma membranes. This effect masks the polyene effect especially for molecules showing a mainly cellular permeation pathway such as amides and lipid soluble molecules.

Acetamides↗