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PubMed1968

Electrical potential and short circuit current of an in vitro preparation of rat colon mucosa.

1. Using a preparation of rat colon mucosa mounted in vitro in small chambers, some factors which influence the electrical properties of the mucosa have been investigated.2. The mucosa behaved mainly as an ohmic resistance although a very brief transient occurred on first passing current. At 32 degrees C, the fresh preparation had a mean resistance of 108Omega/cm(2) and a mean short circuit current (s.c.c.) of 143 muA/cm(2). Tissues taken from Na-depleted and adrenalectomized rats differed little from normal tissues in electrical resistance but those from Na-depleted rats had higher potential difference (p.d.) and s.c.c.3. Increase of temperature led to a rise of conductance of similar order to that found for ions in aqueous solution. S.c.c. also rose with increase of temperature but the effect was relatively greater consistent with its being dependent on metabolic processes.4. Anoxia or the addition of cyanide, iodoacetate or 2,4-dinitrophenol to the bath fluid caused considerable fall in the p.d. and s.c.c.5. Ouabain decreased the p.d. and s.c.c. when added to the serosal side but had no effect when on the luminal side.6. Aldosterone and acetazolamide had no effect.7. Varying serosal side [K] produced only minor changes in p.d.8. Reducing [Na] of the luminal solution caused a considerable fall of p.d. but similar reduction of [Na] on the serosal side had little effect.9. The frequently employed model which represents the transepithelial p.d. as the sum of diffusion potentials originating at the luminal and serosal sides of the cell layer is not consistent with the present results. The colonic transmucosal p.d. probably originates in the electrogenic transport of Na by a mechanism located on the serosal side of the epithelium.

Acetazolamide↗
PubMed1970

Short-circuit current and ionic fluxes in the isolated colonic mucosa of Bufo arenarum.

1. The unidirectional fluxes of (22)Na, (36)Cl and [(14)C]bicarbonate ions were measured in paired portions of the isolated and short-circuited colonic mucosa of Bufo arenarum, separated from its muscular layer. Pharmacological effects as well as effects of changes in the composition of the nutrient solutions on the electrical parameters of membrane activity (potential difference, short-circuit current and total membrane resistance) are described.2. The net fluxes of both Cl and bicarbonate ions were not significantly different from zero in the absence of electrochemical gradients across the membrane.3. The net Na flux from mucosa to serosa represented a variable proportion of the short-circuit current ranging from 62 to 100%.4. The proportion of membranes with high discrepancies between net Na flux and short-circuit current decreased with the duration of captivity of the toads.5. When Na was entirely replaced by choline in the mucosal bathing solution, the short-circuit current dropped by a variable amount within the range of 64 to 98% of its control values in different membranes. This effect was completely reversible. Similar changes in the serosal solution had no effect.6. The short-circuit current and potential difference were very sensitive to the serosal concentration of bicarbonate ions. In different membranes, 60-100% of the short-circuit current was reversibly abolished by bathing the serosal surface with a bicarbonate-free solution. The mucosal bicarbonate level had no effect on either the potential difference or the short-circuit current. 5 mM bicarbonate in the serosal solution restored at least 50% of the short-circuit control value and full recovery was attained by concentrations near 30 mM bicarbonate.7. Anoxia brought the potential difference and short-circuit current reversibly down to zero in about 50 min.8. Ouabain reduced the short-circuit current up to 80% in about 40 min when present in the serosal solution at a concentration of 10(-4)M. At this or lower concentrations the ouabain effect was reversible. Above this level ouabain produced 100% inhibition in 3-4 hr, but this was no longer reversible. Ouabain had no effect on the short-circuit current either when applied to the mucosal surface or in the absence of Na from the mucosal solution.9. Diamox produced a variable inhibition of the short-circuit current of up to 30% only at concentrations above 10 mM.10. Possible mechanisms are discussed for the appearance of the non-Na component of the short-circuit current. A theory concerning its nature is proposed.

Acetazolamide↗
PubMed1979

The transport of the lead cation across the intestinal membrane.

1. The transport of the lead cation has been investigated using the everted sac preparation of Wilson & Wiseman (1954).2. Only a small percentage of lead was transported into the serosal compartment but there was a rapid and massive uptake onto the tissue. There was no significant difference in the amount of lead cations transported across different regions of the small intestine.3. Both the rate of transport into the serosal compartment and the tissue uptake increased linearly with increasing concentration of the lead cation, from 10(-7)M to 5 x 10(-5)M. Little evidence for saturation of serosal transport or tissue uptake was found.4. Lead transport into the serosal compartment appeared to be related to water movement, but was little affected by changes in glucose concentration and temperature.5. It is concluded that lead is transported into the serosal space by a process of passive diffusion linked to water transport.6. The interaction between lead ions and the intestinal tissue was extremely tenacious and displayed characteristics of covalent bonding.7. It is suggested that the lead cation interacts with tissue phosphate ions thus removing lead ions from the transport pool. Chelation of lead to form a neutral species reduces this interaction and also promotes transport.

Animals↗
PubMed1979

Chloride, sodium, potassium and hydrogen ion transport in isolated canine gastric mucosa.

1. The fluxes of isotopically labelled Na+, Cl- and K+ in each direction and H+ secretion across isolated dog gastric mucosa were measured under short-circuit conditions. 2. In the non-stimulated state, the net flux of Na+ was 6.61 micronequiv/cm2.hr from mucosal (luminal, secretory) to serosal (nutrient, blood) side, whereas the net flux of Cl- was only 0.79 micronequiv/cm2.hr, and the direction was from serosal to mucosal side. 3. There was a positive correlation between the net flux of Cl- and acid secretion, however, net flux of Na+ was not correlated with acid secretion initiated by secretagogue treatment. 4. With ion substitution studies, only replacement of mucosal Na+ with choline produced a highly significant decrease in potential difference (p.d.). This indicates that active transport of Na+ from the mucosal to the serosal side is the most important source for the generation of the gastric p.d. in dog gastric mucosa. 5. From ion substitution studies, it was also observed that Cl- in either mucosal or serosal solution is necessary for maintaining acid secretion; whereas only serosal Na+ and K+ are essential for acid secretion. Removal of either Na+ or K+ from the mucosal solution had no effect on acid secretion. 6. Substitution of SO2-(4) for Cl- had no effect on active transport of Na+, but choline substitution for Na+ diminished active transport of Cl-.

Animals↗
PubMed1981

Cellular mechanisms of ion transport associated with osmotic gradients in rat small intestine.

1. The electrical potential difference, short-circuit current, tissue conductance, and fluxes of sodium and chloride were measured in rat small intestine in an in vitro chamber preparation in the presence and absence of 100 mM-mannitol on either the mucosal or serosal surface. 2. Mucosal mannitol generally decreased potential difference, short-circuit current, and tissue conductance while serosal mannitol increased the electrical variables. 3. Mucosal mannitol decreased unidirectional movement of sodium and chloride but did not change the net transport of these ions. The change in short-circuit current was therefore ascribed to changes in fluxes of ions other than sodium and chloride. 4. Serosal mannitol increased the unidirectional fluxes of sodium, but not the new transport of this ion. The transport of chloride increased only in the serosal to mucosal direction yielding a net secretion of chloride equal to the change in short-circuit current. 5. The changes in potential difference and short-circuit current caused by mucosal mannitol were dependent on the presence of sodium. The changes due to serosal mannitol were dependent on both sodium and chloride. 6. Changes in undirectional transport of ions, small non-electrolytes, and water due to an osmotic gradient were attributed to changes in the dimension of the lateral intercellular spaces observed in earlier studies. 7. No evidence suggesting that the electrical changes due to the mannitol gradients could be attributed to diffusive or convective flows of fluid, but instead the changes were ascribed to perturbations in the cellular transport mechanisms.

Animals↗
PubMed1984

Effects of vasopressin on electrolyte transport across isolated colon from normal and dexamethasone-treated rats.

Vasopressin enhanced the absorption of Na+ and Cl- across the short-circuited colon descendens from normal rats. This effect of vasopressin results from an increase in the mucosal to serosal movement of Na+ and Cl- and a decrease in the serosal to mucosal movement of Cl- and was accompanied with a decrease in the short-circuit current (ISC). Neither the base-line absorption of Na+ and Cl-, the vasopressin-induced increase in Na+ and Cl- absorption nor the decrease in ISC were inhibited by amiloride in the colon from normal rats. Colon descendens from rats treated for 3 days with dexamethasone had remarkably higher transmural potential difference (p.d.), tissue conductance (Gt) and ISC. The absorption of Na+ across the short-circuited colon descendens from dexamethasone-treated rats was increased 3-fold when compared to colon from normal rats. The absorption of Cl- in normal rats was reversed to Cl- secretion in treated rats. Amiloride rapidly and reversibly decreased the p.d., Gt and ISC in colon from dexamethasone-treated rats. The transport of Na+ was nearly completely inhibited by amiloride in treated rats. In contrast to its enhancing effects on Na+ absorption in colon from normal rats vasopressin did not enhance Na+ absorption in colon from dexamethasone-treated rats. This enhancement of Cl- absorption by vasopressin was retained in colon from treated rats. This enhancement of Cl- transport was due solely to a decrease in the serosal to mucosal movement of Cl- and was accompanied with a decrease in ISC and Gt. The results support the hypothesis that vasopressin causes inhibition of the electrogenic secretion of Cl- in colon from dexamethasone-treated rats. Furthermore, the results suggest that the increase in the mucosal to serosal movement of Na+ and Cl- and the decrease in the serosal to mucosal movement of Cl- in colon from normal rats are caused by independent effects of vasopressin.

Amiloride↗
PubMed1985

Passive water flows driven across the isolated rabbit ileum by osmotic, hydrostatic and electrical gradients.

Water flows generated by osmotic and hydrostatic pressure and electrical currents were measured in sheets of isolated rabbit ileum at 20 degrees C. Flows across the mucosal and serosal surfaces were monitored continuously by simultaneous measurement of tissue volume change (with an optical lever) and net water flows across one surface of the tissue (with a capacitance transducer). Osmotic gradients were imposed across the mucosal and serosal surfaces of the tissue separately, using probe molecules of various sizes from ethanediol (68 Da) to dextrans (161 000 Da). Flows across each surface were elicited with very short delay. The magnitudes of the flows were proportional to the osmotic gradient and related to the size of the probe molecule. Osmotic flow across the mucosal surface was associated with streaming potentials which were due to electro-osmotic water flow. The mucosal surface is a heteroporous barrier with narrow (0.7 nm radius, Lp (hydraulic conductivity) = (7.6 +/- 1.6) X 10(-9) cm s-1 cmH2O-1) cation-selective channels in parallel with wide neutral pores (ca. 6.5 nm radius, Lp = (2.3 +/- 0.2) X 10(-7) cm s-1 cmH2O-1) which admit large pressure-driven backflows from the submucosa to the lumen. There is additional evidence for a further set of narrow electroneutral pores less than 0.4 nm radius with Lp less than 7 X 10(-9) cm s-1 cmH2O-1. The serosal surface has neutral pores of uniform radius (ca. 6.5 nm), Lp = (7.6 +/- 1.6) X 10(-8) cm s-1 cmH2O-1. Hypertonic serosal solutions (100 mM-sucrose) cause osmotic transfer of fluid from isotonic mucosal solutions into the submucosa, expand it, and elevate the tissue pressure to 19.6 +/- 3.2 cmH2O (n = 4). Conversely, hypertonic mucosal solutions (100 mM-sucrose) draw fluid out of the submucosa in the presence of isotonic serosal solutions, collapse the submucosa, and lower the tissue pressure to -87.7 +/- 4.6 cmH2O (n = 5). Water flows coupled to cation movement could be generated across the mucosal surface in both directions by brief direct current pulses. The short latency of onset and cessation of flow (less than 2 s), absence of polarization potentials, and high electro-osmotic coefficients (range 50-520 mol water F-1), together with the presence of streaming potentials during osmotically generated water flows indicate electro-osmotic water flow through hydrated channels in the tight junctions and/or lateral intercellular spaces.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

The roles of paracellular and transcellular pathways and submucosal space in isotonic water absorption by rabbit ileum.

Water movements have been studied in sheets of isolated rabbit ileum using a method which measures net volume flows across the mucosal and serosal surfaces of the tissue continuously with high resolution. At 35 degrees C, with the tissues incubated in isotonic Ringer solution containing D-glucose (25 mM) on both sides, there is a steady net inflow of fluid at the rate of 24 +/- 2 microliter cm-2 h-1 across the mucosal surface (Jm) and an outflow of 8 +/- 1 microliter cm-2 h-1 across the serosal surface (Js) (n = 16). The stable transepithelial p.d. across these tissues is 2.7 +/- 0.2 mV, serosa positive. Jm can be reversibly inhibited by anoxia. Ouabain (0.1 mM) added to the serosal solution inhibits inflow across the mucosal and serosal surfaces by 75% (n = 7) within 30 min. If phlorizin (0.1 mM) is added to the mucosal Ringer solution containing glucose (20 mM) within 30 min of the commencement of in vitro absorption, Jm is reduced from 37 +/- 3 to 28 +/- 2 microliter cm-2 h-1 (n = 3). Dilution of the mucosal Ringer solution by 50 mosmol kg-1 (with the serosal solution kept isosmolar) results in a rapid transient increase in mucosal inflow. An increase of 50 mosmol kg-1 in the mucosal Ringer solution with NaCl, sucrose or mannitol causes a transient reversal of mucosal flow, followed by a return of inflow at a reduced level. Rabbit ileum can transport water against gradients of approximately 75 mosmol kg-1 of sucrose, NaCl, or mannitol. Addition of polyethylene glycol (mol. wt. 20000; 3 mosmol kg-1) causes a sustained reversal of mucosal inflow; inflow can be restored only by removing polyethylene glycol from the mucosal Ringer solution. The tissue can absorb water against an osmotic gradient of 200 mM-glycerol. The above data have been incorporated into a new model to explain isotonic flow of fluid by this epithelium. The main features are that the hydraulic conductivity (Lp) of the mucosal boundary of the lateral intercellular space is approximately 1 X 10(-8) cm s-1 cmH2O-1. This Lp is too low to sustain isotonicity of the flow emerging from the lateral intercellular space at the observed rates. Hypertonic fluid emerging from the lateral intercellular space is diluted by transcellular water flow generated by the hypertonicity of the submucosa and back-diffusion of solute via mucosal shunt channels.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

The transport of uric acid across mouse small intestine in vitro.

The in vitro recirculation technique was used to study the uptake and transport of uric acid by the jejunum of mouse small intestine. Three components of the serosal secretions appeared to be endogenously derived nucleic acid derivatives; two of these were identified as uric acid and uracil. There was no detectable metabolism of uric acid by the intestine. Uric acid transported from the lumen appeared in the serosal fluid at a concentration higher than that in the lumen. The final serosal/luminal concentration ratio of about 1.18 for exogenous uric acid was found to be constant over the concentration range studied (0.01-0.1 mM). The presence of exogenous uric acid in the lumen did not affect the production of endogenous uric acid by the intestine and its release into the serosal secretions. Mucosal concentration of exogenous uric acid was below, but the total mucosal concentration (exogenous+endogenous) was above, that in the lumen. There was no evidence for the secretion of endogenous uric acid into the lumen. Oxypurinol significantly decreased the rate of serosal appearance of exogenous uric acid. Allopurinol did not affect the transport of exogenous uric acid from the lumen and there was negligible metabolism of allopurinol to oxypurinol by the tissue. Uracil did not affect the transport of exogenous uric acid from the lumen, or the serosal appearance of endogenous uric acid. Likewise uracil transport was unaffected by luminal uric acid.

Allopurinol↗
PubMed1986

The involvement of basolateral potassium channels in the intestinal response to secretagogues in the rat.

The possible involvement of basolateral K+ channels in the intestinal response to secretagogues was investigated using stripped sheets of rat mid-intestine. Increasing the serosal K+ concentration reduced the rise in short-circuit current induced by acetylcholine, 5-hydroxytryptamine, theophylline and prostaglandin E2 (PGE2) without affecting the change caused by glucose. The secretagogue-induced rise in short-circuit current was inhibited by quinine, but not by tetraethylammonium chloride, apamin or 3,4-diaminopyridine. Acetylcholine stimulated 86Rb efflux into the serosal fluid from pre-loaded intestinal sheets and a smaller response was observed with PGE2. The acetylcholine-induced stimulation of 86Rb efflux was inhibited by serosal quinine and lack of serosal Ca2+. Furosemide in the serosal fluid reduced the electrical response to acetylcholine without affecting the increase in 86Rb efflux. It is concluded that as well as increasing luminal Cl- permeability, intestinal secretagogues also enhance the basolateral K+ conductance by activating Ca2+-dependent K+ channels.

Acetylcholine↗
PubMed1988

Electrical transients produced by the toad urinary bladder in response to altered medium osmolality.

1. The effects of changes in media osmolality on the transepithelial current through the toad urinary bladder under voltage-clamp conditions have been studied. Over the limited range (+/- 24 mosmol/kg H2O) used in these investigations, changes in the osmolality of the mucosal bathing fluid produced no changes in transepithelial current. 2. Changes in osmolality of the serosal fluid greatly affected the transepithelial current with a decrease (increase) in osmolality producing a sustained increase (decrease) in current. 3. The changes in steady-state current were approximately proportional to the magnitude of the osmotic steps and were reproducible and reversible if the osmolalities of the solutions were confined to a domain of 220-260 mosmol/kg H2O. 4. Amiloride, which was used to block all active current, also eliminated the electrical responses to an osmotic pulse, indicating that the responses were of cellular origin. 5. The effects of substituting gluconate for medium chloride were examined. Similar responses were observed, indicating that they were not due to changes in a plasma membrane chloride conductance. 6. The transient currents observed during the changes from one steady state to the other often contained an oscillatory component, the amplitude and the degree of damping of which varied between bladders. The amplitude of the oscillations, but not their frequency, could be varied by altering the magnitude of the osmotic pulse and by changing the imposed transepithelial voltage. Decreasing the electrical potential of the mucosal solution with respect to that of the serosal solution decreased the amplitude of the oscillations, as did increased serosal potassium or substitution of gluconate for serosal chloride. The period of the oscillations always remained within the range of 9-12 min. 7. The results suggest that two major processes are initiated by an osmotic step in the serosal bathing medium. The first involves the establishment of new ion gradients and the second, alterations in sodium pump activity. In addition, there is evidence for a voltage-dependent sodium conductance in the apical membrane.

Action Potentials↗
PubMed1989

The transport and metabolism of the uridine mononucleotides by rat jejunum in vitro.

1. Both uridine 3'-monophosphate (3'-UMP) and uridine 5'-monophosphate (5'-UMP) when perfused through the lumen of isolated rat jejunum gave rise to uracil as the only transported pyrimidine appearing in the serosal medium; neither the nucleotide nor the nucleoside could be detected in the serosal fluid. 2. There was a low level of the nucleoside, uridine, in the luminal fluid after the nucleotide had passed through the jejunal segment. Luminal nucleoside appearance was more marked from the 3' form of the nucleotide. 3. The hydrolysis of the nucleotides to the nucleoside form occurred via a brush-border membrane enzyme, which had the same maximal velocity (Vmax) for the two nucleotides (699 +/- 35 and 747 +/- 10 nmol min-1 (mg protein)-1 for 3'-UMP and 5'-UMP, respectively) but a different Michaelis constant (Km) so that 3'-UMP (Km = 58 +/- 3 microM) hydrolysis is favoured over 5'-UMP hydrolysis (Km = 108 +/- microM) at lower concentrations. 4. At 0.05 mM, luminal 3'-UMP gave rise to a higher rate of serosal uracil appearance than luminal 5'-UMP, but at higher luminal concentrations (0.1-0.2 mM) the rate of serosal uracil appearance was the same from both nucleotides. 5. The transmural transport of uracil from the uridine mononucleotides is discussed with reference to the metabolism and compartmentalization of the small intestine responsible for the appearance of the free pyrimidine in the serosal fluid.

Animals↗
PubMed1983

Effects of non-steroidal anti-inflammatory drugs and prostaglandins on alkali secretion by rabbit gastric fundus in vitro.

The effects of non-steroidal anti-inflammatory drugs and prostaglandins E(2) and F(2alpha) on the secretory and electrical activity of isolated rabbit fundic mucosa have been studied. Spontaneous acid secretion was inhibited by serosal side application of sodium thiocyanate (6x10(-2)M) and the resulting alkali secretion measured by pH stat tiration. Serosal side application of indomethacin (10(-5)M) or aspirin (3x10(-3)M) inhibited alkali secretion (0.55+/-0.06 to 0.12+/-0.06 mumol/cm(2)/h, n=6, p<0.01 and 0.28+/-0.06 to 0.11+/-0.03 mumol/cm(2)/h, n=7, p<0.02 respectively). Mucosal or serosal side prostaglandin E(2) (10(-5) to 10(-10)M) and F(2alpha) (10(-4) to 10(-10)M) failed to alter the rate of alkalinisation but secretion was significantly increased by serosal side 16,16-dimethyl-prostaglandin E(2) (10(-6)M) (0.90+/-0.20 to 1.50+/-0.30 mumol/cm(2)/h, n=6, p<0.01). Serosal side application of 10(-6)M prostaglandin E(2) to fundic mucosae pretreated with either aspirin (5x10(-3)M) or indomethacin (10(-5)M), to reduce endogenous E(2) formation, also failed to alter alkali secretion. Pretreatment of the mucosa with 16,16-dimethyl-E(2) (10(-6)M) abolished the inhibitory effect of indomethacin (10(-5)M) on alkali secretion (n=6) but did not modify the secretory response to aspirin (3x10(-3)M) (fall in alkali secretion with aspirin = 81+/-11% and with aspirin plus 16,16-dimethyl-E(2) = 72+/-10%, n=7). In the doses used, none of the prostaglandins or non-steroidal anti-inflammatory drugs altered transmucosal potential difference or electrical resistance. These results show that the damaging agents, aspirin and indomethacin, both inhibit gastric alkali secretion but that modes of action may differ. The observation that prostaglandins, E(2) and F(2alpha) failed to increase alkali production suggests that their protective activity against a variety of damaging agents as shown by others, may be mediated by another mechanism.

Alkalies↗
PubMed1983

Active electrogenic mechanisms for alkali and acid transport in turtle bladders.

Immediately after mounting in the Ussing chamber between choline bicarbonate Ringer solutions devoid of exogenous Na and Cl, the serosal fluid is electronegative to the luminal fluid in bladders from postabsorptive and acidotic turtles; and electropositive in bladders from alkalotic turtles. In bladders from postprandial turtles, the electrical orientation, initially serosal positive, reverses to serosal negative. Serosal additions of 3-isobutyl-1-methylxanthine (IBMX) and adenosine 3',5'-cyclic monophosphate (cAMP) produce no changes in the negative short-circuiting current (Isc) of acidotic turtles but induce large positively-directed increases of Isc in bladders from other turtle groups. With IBMX and cAMP in the (HCO3 + CO2)-rich serosal fluid at pH 7.2 and with luminal pH maintained at 4.0-5.0, the rate at which titratable alkali enters the luminal fluid is electrochemically equal to the positive Isc; and this increased positive Isc is the same as that in the absence of transepithelial gradients. The effects of acetazolamide and 4-acetamido-4-isothiocyanostilbene-2,2'-disulfonic acid on positive and negative Isc are presented. It is concluded that isolated bladders from alkalotic, postprandial or postabsorptive turtles, but not those from acidotic turtles, possess an active electrogenic mechanism for a Na-independent Cl-independent secretion of bicarbonate. This transport process is accelerated by phosphodiesterase inhibitors (IBMX) and cAMP or its eight substituted derivatives.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Electroneutral secretion of bicarbonate by guinea pig gallbladder epithelium.

Transepithelial HCO3- movement in guinea pig gallbladder was investigated in vitro. Absorptive (JHCO3ms) and secretory (JHCO3sm) HCO3- fluxes, determined by use of the pH-stat method were approximately 1.0 and 2.1 mumol X cm-2 X h-1, respectively. The resultant net secretion equaled in magnitude, and balanced electrically, the excess in net absorption of Cl- over that of Na+ X JHCO3sm was dependent on luminal Cl- and serosal Na+; it was inhibited by mucosal 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS; 10(-3) M) and serosal ouabain (3 X 10(-5) M) but not by serosal amiloride (10(-3) M) and scarcely by bilateral methazolamide (10(-4) M). JHCO3ms was reduced by mucosal Cl- but enhanced by serosal Cl-; it was dependent on mucosal Na+ and inhibited by mucosal amiloride and bilateral methazolamide. Our findings are consistent with a model in which 1) serosal HCO3- enters the cell in cotransport with Na+ and is then extruded into the lumen by Cl-(-)HCO3- exchange at the apical membrane; 2) mucosal HCO3- enters the cell secondary to apical membrane Na+-H+ exchange and recycles into the lumen via Cl-(-)HCO3- exchange or is, to a lesser extent, absorbed across the basolateral membrane.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1989

pH effects on basolateral membrane ion conductances in gallbladder epithelium.

The pH sensitivity of the basolateral membrane voltage of Necturus gallbladder epithelial cells (Vcs) was evaluated with conventional and pH-sensitive intracellular microelectrodes. Elevating solution CO2 from 1 to 5% (at constant [HCO3-] = 10 mM) caused a depolarization of Vcs from -76 +/- 3 to -60 +/- 2 mV and a decrease in intracellular pH (pHi) from 7.36 +/- 0.04 to 7.05 +/- 0.03. Serosal exposure to a 50 mM HCO3(-)-5% CO2 solution [at constant extracellular pH (pHo)] caused a similar cell acidification (delta pHi = 0.27), whereas at 3 min Vcs was unchanged. Exposure to 1 mM HCO3- (at constant CO2) depolarized Vcs from -77 +/- 2 to -56 +/- 2 mV and caused a small decrease in pHi (from 7.36 +/- 0.03 to 7.33 +/- 0.03). These results indicate that the observed depolarizations of Vcs are attributable to changes in pHo and not in pHi. Basolateral membrane potassium conductance (GK) congruent to chloride conductance (GCl) congruent to 0.50 mS/cm2 in 10 mM HCO3(-)-1% CO2 Ringer. The depolarization of Vcs caused by elevation of serosal [K+] in 50 mM HCO3(-)-5% CO2 was similar to that observed under control conditions. In contrast, the depolarization of Vcs elicited by elevating serosal [K+] was reduced by about two-thirds in 1 mM HCO3-, whereas the depolarization caused by reduction of serosal [Cl-] was increased twofold in 1 mM HCO3-, compared with control. Inasmuch as the apparent ratio of membrane resistances remained unchanged during serosal solution acidification, the most likely explanation for the observed decrease in Vcs is a reduction of basolateral K+ permeability concomitant with an increase in Cl- permeability.

Animals↗
PubMed1990

Effect of hyperosmotic challenge on basolateral membrane potential in rabbit urinary bladder.

In the rabbit urinary bladder, serosal hyperosmotic challenge (SHOC) with either 33 mM NaCl or 66 mM mannitol caused basolateral membrane potential (Vbl) to initially depolarize from -52.6 +/- 1.6 to -48.4 +/- 1.4 mV, followed by a recovery of Vbl to -57.5 +/- 1.3 mV after 13.7 +/- 1.0 min. The voltage recovery was dependent on both serosal HCO3- and Cl-, and in the absence of both, Vbl depolarized to -11.6 +/- 1.5 mV and the ratio of apical-to-basolateral resistance (Ra/Rbl) decreased from 21.0 +/- 3.4 to 8.3 +/- 3.1. This decrease in Ra/Rbl and consequent depolarization of Vbl is caused by a decrease in basolateral K+ conductance. Replacement of serosal Cl- with NO3- or SCN- followed by SHOC caused a sustained depolarization of Vbl to -32.5 +/- 4.4 and -40.9 +/- 0.9 mV, respectively. However, when Br- was used to replace Cl-, voltage recovery occurred but was slowed (24.0 +/- 2.7 min) and reduced in magnitude (-47.5 +/- 3.5 mV). Addition of amiloride (1 mM) or niflumic acid (100 microM), but not bumetanide (1 microM), to the serosal bathing solution inhibited voltage recovery causing Vbl to depolarize to -36.3 +/- 2.6 and -41.5 +/- 4.5 mV, respectively. Serosal addition of ouabain after SHOC caused Vbl to depolarize by 10.8 +/- 0.9 mV in 2 min. We speculate that the SHOC-induced initial depolarization of Vbl is a loss of Ba2(+)-sensitive K+ conductance caused by cell shrinkage. The subsequent repolarization/hyperpolarization of Vbl is caused by an enhanced basolateral membrane Na+ pump current and a reappearance of the Ba2(+)-sensitive K+ conductance. The parallel operation of Na(+)-H+ and Cl(-)-HCO3- exchanges will then supply Na+ for the pump current and, via cellular accumulation of Na+, K+, and Cl-, might result in a partial recovery of cell volume and thus Ba2(+)-sensitive K+ conductance.

Amiloride↗
PubMed1990

Furosemide blocks basolateral membrane Cl- permeability in gallbladder epithelium.

In Necturus gallbladders bathed in a NaCl Ringer solution buffered with 10 mM HCO3(-)-1% CO2, furosemide (added to the serosal solution) caused a concentration-dependent hyperpolarization of both cell membranes that was slow and reversible. At 10(-3) M furosemide, the basolateral membrane voltage (Vcs) increased significantly from -71 +/- 3 to -85 +/- 3 mV, the depolarization of Vcs elicited by a 10-fold rise in serosal [K+] increased from 34 +/- 4 to 50 +/- 1 mV, the depolarization elicited by lowering serosal [Cl-] from 98 to 8.1 mM was reduced from 15 +/- 1 to 1 +/- 1 mV, and the depolarization in response to lowering serosal [HCO3-] from 10 to 1 mM was reduced from 13 +/- 1 to 5 +/- 0.4 mV. Furosemide could in principle decrease the basolateral membrane Cl- conductance (Gcl), increase the basolateral membrane K+ conductance, or have a combined effect. To distinguish among these possibilities, we estimated the resistance of the basolateral membrane (Rb) by means of two-point intraepithelial cable analysis experiments. Furosemide increased Rb by 22%, which indicates that furosemide reduces basolateral membrane Gcl. The effect cannot be attributed to inhibition of apical membrane anion exchange by serosal addition of furosemide, because base secretion from cells to lumen is unchanged. We conclude that furosemide blocks reversibly basolateral membrane electrodiffusive Cl- permeability. A concomitant stimulation of basolateral membrane electrodiffusive K+ permeability is also possible.

Animals↗