scholarly journals The gravitation-driven stress-reduced urothelial barrier in toad bladder urothelium

2021 ◽  
Author(s):  
Xinli Tan ◽  
Danmei Wang ◽  
Shouyan Fan ◽  
Xiaochi Xu ◽  
Hui Guo ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Urinary Bladder ◽  
Tight Junction ◽  
Chloride Channels ◽  
Transmembrane Potential ◽  
Electrical Potential ◽  
Potential Difference ◽  
Variation Method ◽  
Apical Side ◽  
Transmembrane Potential Difference

The urinary bladder urothelial are highly specialized epithelia that protect the underlying tissues from mechanical stress and seal them from the overlying fluid space. To better understand the maintaining permeability induced electrical potential roles played by urothelial in the bladder, we established a protocol of gravitation stress in toad urothelial, observed the transmembrane potential difference variation. Method: The toad urothelial were mounted in a using chamber which the chamber was separated to two solution spaces, and stable with 0.9% saline solution. The electrodes were settled on the surface of each side of the preparation, serosal side definite as cathode. The using chamber was settled in the centrifugal rotor and under 300 rpm rotation to obtain a vertically +4G gravitation on serosal chamber 5min. Result: a transient transmembrane potential difference increasing was observed after adding CaCl2 (3% solution) in serosal chamber. The amplitude increasing phase included a rapid and a slowly ascending phase. In gravitation stressed urothelial preparation, CaCl2 induced transient phase was significantly increased, furthermore the secondary slowly ascending phase was much more amplified on its amplitude axis and significantly prolonged on the time scale than that evoked in control preparations. The evoked total amplitude increasing were 10 times higher than that in control. Conclusion: The urinary bladder epithelial layer has a structure which regulates ion permeability as a barrier. The tight junction plays an important role as the intercellular coupling in the apical side of the epithelial cell. On the other hand, it is known that the ion channel exists on the epithelial cell membrane and regulates the physiological process. The gravitation stress weakened the tight junction. The transmembrane potential difference was enhanced both on its amplitude and prolonged time. The gravitation stress induced hyperpolarization that evoked by CaCl2 is one kind of Cl- transfer from serosal chamber in which high Ca2+ in the urothelial basal membrane activated the calcium-activated chloride channels. This outwardly rectifying chloride channel induced hyperpolarization can be blocked by Nppb.

Ion fluxes considered in terms of membrane-surface electrical potentials

2001 ◽  
Vol 28 (7) ◽  
pp. 607 ◽  
Author(s):  
Thomas B. Kinraide
Keyword(s):  
Plasma Membranes ◽  
Transmembrane Potential ◽  
Chemical Potential ◽  
Membrane Surface ◽  
Electrical Potential ◽  
Bulk Phase ◽  
Potential Difference ◽  
Bathing Medium ◽  
Electrical Potentials ◽  
Transmembrane Potential Difference

Ions transported through plasma membranes encounter electrical charges, and associated electrical potentials, at the membrane surfaces. The ionic composition of the tissue-bathing medium influences both the surface charge density and the surface electrical potential. Changes in surface electrical potential may affect ion transport by altering two components of the chemical potential difference (Δµj ) of an ion through the membrane. First, the surface activity of the transported ion will change because of electrostatic attraction or repulsion. Second, the surface-to-surface transmembrane potential difference will change. (This is different from the bulk-phase-to-bulk-phase transmembrane potential difference measured with microelectrodes.) These changes in the components of the chemical potential may change the flux of an ion through the membrane even if the surface-to-surface Δµj (equal to the bulk-phase-to-bulk-phase Δµj ) remains constant. The Goldman-Hodgkin-Katz (GHK) flux equation does not take into account these surface-potential effects. The equation has been modified to incorporate surface potentials computed by a Gouy-Chapman-Stern model and surface ion activities computed by Nernst equations. The modified equation (despite several additional deficiencies of the GHK model) successfully predicts many transport phenomena not predicted by the standard GHK equation. Thus electrostatic effects may account for saturation, cis- and trans-inhibition, rectification, voltage gating, shifts in voltage optima, and other phenomena also attributable to other mechanisms.

D-glucose uptake is increased in jejunal brush-border membrane vesicles from hyperthyroid chicks

1989 ◽  
Vol 120 (4) ◽  
pp. 435-441 ◽  
Author(s):  
Hanna Debiec ◽  
Heide S. Cross ◽  
Meinrad Peterlik
Keyword(s):  
Glucose Uptake ◽  
Glucose Transport ◽  
Brush Border ◽  
Transmembrane Potential ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Potential Difference ◽  
Daily Injection ◽  
Transmembrane Potential Difference

Abstract. Jejunal brush-border membrane vesicles were harvested from 4-week old chicks whose thyroid status had been altered either by a daily injection of 20 μg T3 for 1 week or which through the preceding 4 weeks had received propylthiouracil and than had been repleted with either 20 or 80 μg T3 in divided doses within 48 h. T3 markedly stimulated D-glucose uptake in brush-border membrane vesicles in the presence of an outside/inside (100/0 mmol/l) Na+ gradient. T3 administration had no detectable influence on the Na+ permeability of the isolated vesicles. The effect of the thyroid hormone on Na+ gradient-driven D-glucose uptake was fully preserved at zero transmembrane potential difference. These findings exclude that T3 stimulates Na+-dependent D-glucose transport in the small intestine through changes of the electrochemical Na+ gradient or through alteration of the transmembrane potential difference. Tracer exchange experiments under equilibrium and voltageclamp conditions revealed a significantly shorter halftime of D-glucose uptake in brush-border membrane vesicles from T3-treated chicks. Kinetic analysis showed that T3 administration significantly increases the apparent maximal velocity of D-glucose transport in brushborder membrane vesicles, whereas the apparent Km values were virtually unaltered. From these data we conclude that T3 increases the activity of Na+-dependent D-glucose carriers in the brush-border membrane. This is interpreted as consistent with a greater rate of D-glucose absorption from the intestinal lumen under conditions of hyperthyroidism.

Hepatic taurocholate uptake is electrogenic and influenced by transmembrane potential difference

1993 ◽  
Vol 264 (3) ◽  
pp. G478-G485 ◽  
Author(s):  
S. D. Lidofsky ◽  
J. G. Fitz ◽  
R. A. Weisiger ◽  
B. F. Scharschmidt
Keyword(s):  
Electrical Potential ◽  
Membrane Depolarization ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Perfused Liver ◽  
Cultured Hepatocytes ◽  
Patch Clamp Recording ◽  
Intracellular Microelectrodes ◽  
Transmembrane Electrical Potential ◽  
Transmembrane Potential Difference

Uptake of the bile acid taurocholate by hepatocytes is coupled to Na+ influx. The stoichiometry of uptake, however, is uncertain, as is the influence of the transmembrane electrical potential difference (PD) on this process. In this study, we examined the relationship between taurocholate extraction and PD (measured using intracellular microelectrodes) in perfused liver, and we measured taurocholate-induced transport current in cultured hepatocytes using patch-clamp recording techniques. In the perfused liver under basal conditions, PD averaged -28.4 +/- 0.6 (SE) mV, and extraction of 1, 50, and 300 microM taurocholate was 0.95 +/- 0.02, 0.98 +/- 0.01, and 0.41 +/- 0.03, respectively. When the Na+ chemical gradient was decreased by replacing perfusate Na+ with choline, the membrane depolarized to -17.2 +/- 1.1 mV, and taurocholate extraction markedly decreased at all taurocholate concentrations (P < 0.01). When perfusate Na+ concentration was held constant at 137 mM, membrane depolarization induced by substitution of gluconate for perfusate Cl- (-17.9 +/- 0.6 mV) or Cl- for nitrate (-10.3 +/- 2.1 mV) significantly decreased extraction of 300 microM taurocholate. Abrupt exposure to taurocholate produced a concentration-dependent membrane depolarization in the presence of Na+, but not in its absence (P < 0.001). In cultured hepatocytes, exposure to 100 microM taurocholate produced an inward current of -0.056 +/- 0.016 pA/pF at a holding potential of -40 mV. This current was Na+ dependent, and it increased twofold as holding potential was changed from -20 to -50 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of transmembrane potential differences of renal tubular epithelial cell on ANG II binding

1987 ◽  
Vol 252 (2) ◽  
pp. F209-F214 ◽  
Author(s):  
G. P. Brown ◽  
J. G. Douglas
Keyword(s):  
Glucose Uptake ◽  
Time Course ◽  
Transmembrane Potential ◽  
Membrane Vesicles ◽  
Potential Difference ◽  
Scatchard Analysis ◽  
Ang Ii ◽  
Sodium Salts ◽  
Sodium Dependent ◽  
Transmembrane Potential Difference

Previous studies from this laboratory demonstrated specific high-affinity binding sites of rat renal brush-border membrane vesicles (BBMV). The time course of angiotensin II (ANG II) binding in the presence of a NaCl gradient (medium greater than intravesicular) demonstrated an "overshoot" characteristic of electrogenic sodium-dependent D-glucose uptake. The time course of ANG II binding to membrane vesicles equilibrated with NaCl did not exhibit such "overshoot" and was lower in magnitude. Therefore, studies were designed to test the hypothesis that ANG II binding to BBMV was enhanced by a transmembrane potential difference in a manner similar to sodium-dependent D-glucose uptake. The effects of sodium salts with differing rates of anion equilibration were compared on ANG II binding. Peak binding was achieved most rapidly with NaSCN followed by NaCl and Na2SO4. By contrast, sodium acetate, which is translocated electroneutrally, exhibited no overshoot. ANG II binding in the presence of a KCl gradient was similar to NaCl. The overshoot was abolished in the presence of an inwardly directed KCl gradient plus valinomycin. Magnesium salts with differing rates of anion permeabilities had similar effects on binding, as did sodium salts. Scatchard analysis revealed that the receptor density was fourfold higher in the presence of an electrochemical gradient compared with nongradient conditions. These data are consistent with the conclusion that ANG II binding to BBMV is enhanced by a transmembrane potential difference, and suggest that this may be an important modulator of tubular epithelial responses to ANG II in vivo.

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