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S Curci

Publications and source records attributed to S Curci.

10 recordsLinked to original sources
PubMed1992

Microelectrode determination of oxyntic cell pH in intact frog gastric mucosa. Effect of histamine.

Intracellular pH (pHi) of acid-secreting cells was measured in intact gastric fundus mucosa of Rana esculenta with double-barrelled pH microelectrodes. Tissues were mounted, serosal side up, between two half chambers and individual cells were impaled after microsurgical removal of the serosal muscle layer. Transepithelial potential difference (Vt) and resistance (Rt) as well as serosal cell membrane potential (Vs) and pHi were continuously recorded at rest (0.1 mmol/l cimetidine) or during stimulation (0.5 mmol/l histamine). During chamber perfusion with HCO3-/CO2-buffered Ringer solution of pHo = 7.36, Vt and Rt were -21.7, SD +/- 6.0 mV and 229 +/- 83 omega cm2 (n = 17) while Vs and pHi averaged -57.3 +/- 6.9 mV and 7.4 +/- 0.11 (n = 25). The latter value is considerably more alkaline than all recent pHi measurements obtained with microspectrofluorometric techniques on isolated cells, glands or intact tissue. The difference may in part be explained by use of HCO3(-)-free solutions in most of the previous studies because we observed that such solutions decrease pHi to 6.89 +/- 0.18 (n = 4). Again, in contrast to recent literature, application of histamine in HCO3-/CO2-buffered solution led to further transient alkalinization by 0.12 +/- 0.05 pH unit (n = 8). Since in accidental punctures of the gastric gland lumen we noticed that H+ secretion only began approximately 5 min after histamine application, we conclude that the histamine-induced initial alkalinization does not reflect stimulation of the H+/K+ ATPase pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Comparison of the basolateral K+ conductance of the epithelial cells in frog gastric fundus mucosa.

Frog stomach transepithelial potential difference (Vt) and resistance (Rt) as well as the voltage divider ratio (VDR) and serosal membrane potential (VS) of surface epithelial (SEC) and oxyntic (OC) cells were recorded at rest and during stimulation with histamine. Serosal membrane K+ permeability was tested by sudden elevation of serosal K+ concentration from 4 to 13 mmol l-1. Stimulation decreased both Vt and Rt and increased VDR of the OC (from 9.4 +/- SD 3.0 to 14.4 +/- 4.1, n = 10, P less than 0.001), while VS remained virtually unchanged (-66.3 +/- 4.5 mV, n = 10); in SEC, however, VDR as well as VS increased, the latter from -67.3 +/- 5.9 to -75.7 +/- 7.3 mV, n = 9, P less than 0.001. Elevation of serosal K+ reversibly diminished Vt and Vs in both cell types. The transepithelial response to K+ increased after stimulation. However, the cell potential response delta Vs,K increased only in the SEC (from +16.0 +/- 2.9 to +18.5 +/- 2.6 mV, n = 9, P less than 0.001) but not significantly in the OC. We conclude that in frog stomach both OC and SEC are stimulated by histamine: the SEC respond with a hyperpolarization, which reflects an increase in their basolateral K+ conductance; the OC do not respond with a hyperpolarization, possibly because histamine increases the basolateral membrane K+ conductance as well as other ion conductances which have not yet been identified.

Animals↗
PubMed1990

Effect of histamine on the basolateral K+ conductance of frog stomach oxyntic cells and surface epithelial cells.

The transepithelial potential difference (Vt) and resistance (Rt) and the basolateral cell membrane potential (Vs) of oxyntic cells (OC) and surface epithelial cells (SEC) were measured in isolated stomachs of Rana esculenta. At rest, Vs of OC and SEC was virtually identical [-66.3 +/- 4.5 (SD) (n = 10) and -67.3 +/- 5.9 mV (n = 9)] and both cells responded to increasing serosal K+ concentration from 4 to 13 mmol/l with virtually the same depolarization (delta Vs,K) of +16.2 +/- 2.0 and +16.0 +/- 2.9 mV, respectively, while Vt declined by approximately half as much. Histamine (0.1 mmol/l) reduced Vt and Rt and increased the voltage divider ratio in both cell types, indicating a fall in basolateral membrane resistance. In the OC, this increase was neither associated with a significant alteration of Vs nor with a change in delta Vs,K. In the SEC, however, histamine markedly increased Vs to -75.5 +/- 7.3 mV (n = 9) as well as delta Vs,K to +18.5 +/- 2.6 mV, which was paralleled by an increase in delta Vt,K from 9.8 +/- 3.9 to +12.8 +/- 4.2 mV. The data indicate that 1) both OC and SEC respond to histamine, 2) both OC and SEC contain a basolateral K+ conductance that increases under histamine (in OC probably, in parallel with other ion conductances), and 3) in Rana esculenta the SEC contribute substantially to Vt.

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↗