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PubMed1997

Fluid recirculation in Necturus intestine and the effect of alanine.

Fluid absorption by Necturus small intestine has been studied using radiolabeled dextrans as molecular probes of the paracellular pathway under voltage-clamped conditions. Fluxes of H3-dextrans of MW up to 20K were followed in both directions between mucosal (M) and serosal (S) baths by fractionating those that passed the epithelium as a function of molecular radius. Consideration of the unstirred layers in the baths and the surface geometry rules out any contribution made by solute polarization. The geometry of the paracellular system was measured by light microscopy, TEM and SEM, and values were used in conjunction with a program that calculates convective-diffusive coupling in the tight junctions, intercellular spaces and subepithelium in series. The results indicate that the net fluxes are due to the convection of fluid through two opposing paracellular fluid circuits with different size selectivity, resulting in net absorption at small radii. Alanine at 20 mM stimulates fluid and salt uptake by a factor of 2. Its effect on the two convective components is to increase the M to S flux and decrease the S to M. The selectivities are not significantly different from those before alanine treatment. The volume absorption predicted from the net probe fluxes is very close to that measured gravimetrically across the epithelium.

Alanine↗

PubMed1998

Improved intraepithelial two-dimensional cable analysis with application to necturus gastric antral mucosa.

Previously 2D cable analysis has been performed with two microelectrodes, one for passing intraepithelial current and the other for measuring the voltage response in multiple cells along the distance scale. This requires that the epithelium must be in a stable state for a considerably long period because of the multiple impalements. To follow changes of intraepithelial resistances in chambered Necturus antral mucosa with good temporal resolution, four/five electrodes were used to impale cells in the same preparation and the intraepithelial current (6.5-20 nA) was conducted sequentially to three/four of the electrodes, one at a time, to obtain six/ten independent voltage response measurements along the distance scale. The solution to the 2D cable equations was fitted to results and apical, basolateral and shunt resistances were calculated. It was found that an incorrect distance configuration can ruin the precision of the measurement. The distance configuration can, however, be optimized. The resistance values calculated with the 2D cable analysis were very close to those obtained by the amiloride exposure technique in the same tissues. The improvement gained with this work is better temporal resolution (even <10 s) when measuring epithelial resistances.

Amiloride↗

PubMed1999

The activation of an apical Cl- conductance by extracellular ATP is potentiated by genistein in Necturus gallbladder epithelium.

Necturus gallbladder epithelium (NGE) expresses a CFTR-homologous apical Cl- conductance (Ga,Cl) which can be activated either by elevation of intracellular cAMP or by extracellular ATP. Here we show by microelectrode experiments and impedance analysis that genistein (50 microM), which is known to potentiate the stimulation of Ga,Cl in several cell culture models, also potentiates the stimulation of Ga,Cl by low doses of forskolin in NGE. Moreover, we show that genistein also potentiates the stimulation of Ga,Cl by ATP. In addition genistein renders gallbladders that initially do not respond to ATP sensitive to this stimulant, and it delays the conductance inactivation after ATP removal. Under control conditions Ga,Cl inactivates within < 5 min, but in the presence of genistein a significant Ga,Cl persists even after 60 min. These effects of genistein are not related to inhibition of protein tyrosine kinases, since structurally different inhibitors of the tyrphostin family do not mimic the genistein effects. The data support our conclusion that stimulation of Ga,Cl by ATP is mediated by activation of the cAMP pathway and involves a CFTR-homologous protein. They also favour the view that genistein acts via inhibition of protein phosphatases which dephosphorylate CFTR, but cannot exclude the possibility of a direct interaction with CFTR.

Adenosine Triphosphate↗

PubMed1999

Activation of an apical Cl- conductance by extracellular ATP in Necturus gallbladder is mediated by cAMP and not by [Ca2+]i.

Necturus gallbladder epithelium (NGE) expresses a CFTR-like apical Cl- conductance that can be activated by cAMP. Here, we show that extracellular ATP (100 microM), which is known to elevate intracellular Ca2+ and to hyperpolarize cells by stimulating apical and basolateral K+ conductances, also stimulates an apical Cl- conductance (Ga,Cl), however with a much slower time course. The selectivity sequence of Ga,Cl was SCN- > I- > NO3- > Br- > Cl- >> isethionate (ISE-), but SCN- and I- partially blocked it, which is analogous to observations of CFTR Cl- channels. To disclose a possible role for intracellular Ca2+, gallbladders were incubated with the Ca2+ chelator BAPTA/AM or bathed in solutions containing only submicromolar Ca2+ concentrations. BAPTA partially inhibited the Ca(2+)-mediated hyperpolarization, but did not reduce the ATP-dependent activation of Ga,Cl and the latter was also seen in low extracellular Ca2+. On the other hand, the cAMP-antagonist Rp-8-Br-cAMPS strongly inhibited the stimulation of Ga,Cl by ATP (as well as by forskolin), but left the ATP-induced hyperpolarization unchanged. Preincubation with a low concentration of forskolin markedly enhanced the stimulatory effect of ATP, and this effect was not modified by the selective inhibition of protein kinase C. These data suggest the involvement of different signal transduction pathways in the ATP-dependent activation of K+ and Cl- conductances in NGE. The stimulation of the Ga,Cl appears to be mediated by cAMP but not by elevation of intracellular Ca2+.

Adenosine Triphosphate↗

PubMed1989

Effects of aspirin and acetic acid on intracellular pH in necturus gastric mucosa.

Intracellular microelectrode techniques were employed to examine the effects of luminal aspirin and acetic acid on intracellular pH and cell membrane potential in the surface epithelial cells of Necturus antrum. Antral mucosa was mounted in a modified Ussing chamber, and intracellular pH was determined from the difference between the potentials recorded by intracellular conventional and pH-sensitive microelectrodes. Under neutral conditions (pH7), aspirin (5 mM) hyperpolarized (-7.5 +/- 1 mV, p less than 0.0001) and acetic acid (5 mM) depolarized (+4 +/- 0.08 mV, p less than 0.001) cell membrane potential. Neither agent had any significant effect on intracellular pH. Under acidic conditions (pH 4.5), aspirin (5 mM) reduced the intracellular pH from 6.99 +/- 0.03 to 6.87 +/- 0.04 (p less than 0.001) and depolarized cell membrane potential from -36.7 +/- 1.5 to -30.3 +/- 1.6 mV, p less than 0.001). Similarly, acetic acid (5 mM) acidified the cells (-0.20 +/- 0.02, p less than 0.001) and depolarized cell membrane potential (+9.6 +/- 1.9 mV, p less than 0.01). These changes suggest that, in the absence of luminal acid, small organic acids, such as aspirin and acetic acid, may have complex effects on the ionic conductances of the surface cell membranes without altering intracellular pH. In contrast, under acidic conditions, these agents increase the permeability of the apical cell membrane-to-acid back-diffusion from the gastric lumen.

Acetates↗

PubMed1984

Permeability properties of the subepithelial tissues of Necturus gallbladder.

The permeability properties of the subepithelial connective tissue of Necturus gallbladder were evaluated by measurement of electrical resistance, dilution potentials and hydraulic water permeability. The gallbladder epithelial cells were removed by scraping and the underlying connective tissue placed in an Ussing chamber. The electrical resistance was 2.2 +/- 0.8 omega X cm2; the tissue was slightly cation selective relative to free solution. The subepithelial tissues restricted the rate of diffusion of small solutes to 50% of the free solution value. The hydraulic water permeability averaged 2.1 X 10(-2) cm/s per atm. We conclude that limitations of the area of subepithelium available for fluid movement are the most important factors in determining the restrictions to solute and water flow offered by the subepithelial tissues.

Animals↗

PubMed1986

Effect of hypertonicity on the increase in basolateral conductance of Necturus small intestine in response to Na+-sugar cotransport.

Exposure of Necturus small intestine to a galactose-containing perfusate that is 20% hypertonic compared to the galactose-free (control) perfusate results in a rapid depolarization of the electrical potential difference across the apical membrane, psi mc, and a decrease in the ratio of the resistance of the apical membrane to that of the basolateral membrane, (rm/rs); however, the slow repolarization of psi mc and increase in (rm/rs), observed under isotonic conditions, is blocked. These findings are consistent with the notion that the increase in the conductance of the basolateral membrane in response to Na+-coupled sugar (or amino acid) transport across the apical membrane may be a 'volume regulatory response' to cell swelling.

Animals↗

PubMed1987

Changes in the apparent chloride permeability of Necturus enterocytes during the sodium-coupled transport of alanine.

The membrane potential and intracellular Cl- activity of Necturus enterocytes were measured with double-barrelled ion-selective microelectrodes and apparent permeability coefficients (PCl) for the apical membrane calculated from Cl(-)-replacement experiments. In the presence of L-alanine in the mucosal solution an increase in PCl took place. It is proposed that this might reflect the activation of a Cl- conductance during active substrate transport.

Alanine↗

PubMed1987

Electrophysiology of L-lysine entry across the brush-border membrane of Necturus intestine.

Microelectrode measurements of apical membrane potentials (Va) in absorptive cells of isolated Necturus intestine showed that, in the presence or absence of external Na+, 10 mM lysine added to the mucosal medium caused rapid depolarization followed by slower repolarization of Va. In Na+-free media the effects of 10 mM lysine on Va were abolished by 10 mM leucine which alone had no effect on Va under these conditions. This indicates that uncoupled electrodiffusion of lysine plays little or no role in lysine entry across the brush-border membrane. When external Na+ was greater than 10 mM the maximum depolarization of Va (delta Va') induced by [Lys] ranging from 5 to 30 mM was a simple saturable function of [Lys]. In Na+-free media, the relationship between delta Va' and [Lys] was biphasic. At first, delta Va' increased with increasing [Lys] reaching a maximum at 10 mM lysine. When [Lys] was further increased, delta Va' declined progressively to reach zero or near zero values. A single transport pathway model is proposed to account for rheogenic lysine entry across the brush-border membrane in the presence and absence of Na+. This postulates an amino acid transporter in the membrane with two binding sites. One is an amino acid site specific for the alpha-amino-alpha-carboxyl group. The other is a Na+ site. Neutral amino acids (e.g. leucine) compete with lysine for the amino acid site. The Na+ site has some affinity for the epsilon-amino group of lysine. When external Na+ is high the Na+ site is essentially 'saturated' with Na+ and formation of a mobile complex between an amino acid and the transporter depends in a saturable fashion on amino acid concentration. In Na+-free media or in media containing low [Na+]; at low external [Lys] the epsilon-amino group of a lysine molecule (simultaneously attached to the amino acid site) interacts with the Na+ site to form a mobile complex, as external [Lys] is increased, attachment of different lysine molecules to each site of an increasing number of transporters to form nontransported or poorly transported complexes results in substrate inhibition of the rheogenic lysine transport process.

Amino Acids↗

PubMed1988

K+ channels activated by L-alanine transport in isolated Necturus enterocytes.

Using the patch-clamp technique, we demonstrate here the opening of K+ channels evoked by the actively transported amino acid L-alanine in isolated Necturus enterocytes. These channels had a conductance of about 30 pS and their activation was dependent on transmembrane electrical potential and cytosolic Ca2+.

Alanine↗

PubMed1987

Effects of luminal hyperosmolality on cellular and paracellular ion transport pathways in necturus antrum.

Using microelectrode techniques, the electrical properties of the cell membranes and paracellular pathway of the surface epithelium in Necturus antrum were studied under control conditions and during exposure to mucosal solutions made hyperosmotic by addition of sucrose or urea. Sucrose (500 mmol/kg) significantly decreased apical membrane resistances (Ra, from 5501 +/- 841 to 3789 +/- 597 omega X cm2, p less than 0.01), and basolateral membrane resistances (Rb, from 3805 +/- 646 to 2594 +/- 429 omega X cm2, p less than 0.05). The paracellular pathway resistance (Rs) increased significantly from 720 +/- 57 to 822 +/- 71 omega X cm2 (p less than 0.001). Urea (500 mmol/kg) more markedly diminished the apical and basolateral resistances (Ra, from 4303 +/- 663 to 1914 +/- 286 omega X cm2, p less than 0.001; and Rb, from 2600 +/- 474 to 1034 +/- 213, p less than 0.001). In contrast to sucrose, urea-containing solutions significantly decreased Rs (from 682 +/- 78 to 398 +/- 57 omega X cm2, p less than 0.001). Electron micrographs revealed dilatation of lateral intercellular spaces and disruption of desmosomes in tissues exposed to urea, but no visible alterations in tissues exposed to solutions containing sucrose. The resistance of the cellular pathway to ion permeation was thus diminished during exposure to both solutes. In contrast, changes in resistance of the paracellular pathway appeared to depend on the effects of each solute on dimensions and structures of the intercellular pathways.

Animals↗

PubMed1988

Intracellular pH in isolated Necturus antral mucosa in simulated ulcerogenic conditions.

Intracellular pH (pHi) was measured with proton-sensitive liquid sensor microelectrodes in isolated Necturus antral mucosa, paying special attention to arranging experimental conditions to simulate conditions frequently associated with in vivo "stress ulceration." Intracellular pH in mucosas perfused under standard conditions (Ringer's solution containing HCO3-/CO2) was 7.22 + 0.02 (n = 27). Removal of Na+ and HCO3- or addition of amiloride or 4-acetamido-4-isothiocyanostillbene-2,2-disulfonic acid (blockers of Na+/H+ and Cl-/HCO3-exchangers) had no influence on steady-state pHi, suggesting that these ion exchangers do not significantly contribute to the maintenance of pHi in the presence of normal external pH. Acidification of mucosal (luminal) perfusate to pH 3 (mimicking the presence of gastric acid) had no influence on pHi, but mucosal pH 2 (10 mM HCl) acidified pHi to 6.93 +/- 0.07. Acidification of serosal (nutrient) perfusate to pH 6 (mimicking intramucosal acidosis caused by back-diffusion of luminal H+) acidified pHi to 6.72 +/- 0.10. Removal of Na+ from and addition of amiloride to the serosal perfusate during exposure to serosal pH 6.0 induced further acidification of pHi, suggesting that in this acidotic situation (with very low ambient HCO3- concentration) a Na+/H+ exchanger does contribute to the maintenance of steady-state pHi. Increased PCO2 (10% vol/vol in the gas) in a slightly acidic milieu (mimicking mucosal ischemia) likewise acidified pHi to 6.73 +/- 0.05. A combination of mucosal acid (pH 3), high PCO2 (10% CO2), and low serosal pH (pH 6) (mimicking conditions that prevail, for example, during hemorrhagic shock) acidified pHi and ultimately resulted in cell death. These derangements of intracellular acid-base balance may have pathogenetic importance also in in vivo stress ulceration.

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

PubMed1989

Effect of barrier-breaking agents on intracellular pH and epithelial membrane resistances: studies in isolated Necturus antral mucosa exposed to luminal acid.

Features of "H+ back-diffusion" after disruption of the gastric mucosal barrier were investigated by assessing, with a microelectrode technique, the influence of three barrier-breaking agents, taurocholate (10 mM), ethanol (20% vol/vol), and acetylsalicylic acid (10 mM) on intracellular pH and epithelial membrane potentials and resistances in isolated Necturus antral mucosa exposed to luminal acid (pH 3). Exposure of the mucosa to each of the three agents induced intracellular acidification of surface epithelial cells, but the pattern of pHi behavior was different for each agent: taurocholate induced immediate acidification of pHi, ethanol acidified pHi after a delay of 4-6 min, whereas acetylsalicylic acid initially alkalinized pHi, whereafter a rapid acidification of pHi occurred. Assessment of intraepithelial membrane resistances indicated that taurocholate primarily increases cellular conductance, decreasing in particular Ra. In contrast, ethanol mainly increased paracellular conductance, but also decreased cellular resistance, in particular Ra. Acetylsalicylic acid initially increased cell membrane resistances and Ra/Rb, whereafter a rapid decrease of Ra/Rb and Rt occurred. In each instance, the decrease of Ra/Rb preceded acidification of pHi. The data suggest that all three agents induce intracellular acidification by increasing the conductance of the apical cell membrane to H+, but in ethanol-treated tissues paracellular conductance primarily contributes to H+ back-diffusion.

Animals↗

PubMed1990

Intracellular pH in isolated Necturus antral mucosa exposed to luminal acid.

Regulation of intracellular pH in gastric epithelial surface cells exposed to luminal acid was investigated in isolated Necturus antral mucosa using microelectrode technique. Exposure of the mucosa to luminal pH 2 acidified intracellular pH from 7.21 +/- 0.01 to 6.95 +/- 0.04 (N = 50). Removal of Na+ from the perfusates or addition of amiloride (1 mM) to serosal perfusate (containing HCO3-) had no influence on intracellular pH during exposure to pH 2 (N = 6), but removal of HCO3-/CO2 from or addition of 4, acetamido-4-isothiocyanatostilbene-2,2-disulfonic acid (0.5 mM) to the serosal perfusate (containing Na+) acidified intracellular pH from 7.02 +/- 0.03 to 6.45 +/- 0.15 (p less than 0.01, N = 10) and from 6.97 +/- 0.06 to 6.58 +/- 0.26 (p less than 0.01, N = 6), respectively, in 15 min. In tissues exposed to mucosal pH 6, epithelial surface pH was about 1.3 pH units higher than pH of the mucosal bulk solution. Removal of Cl-/HCO3- from the serosal perfusate acidified epithelial surface pH by about 0.5 pH units (p less than 0.01, N = 6), suggesting that serosal HCO3- sustains intracellular pH, at least in part, by generating an alkaline buffer layer at the epithelial surface. In the absence of HCO3-/CO2, a stable intracellular pH was obtained when the tissue was exposed to mucosal pH 2.7, but in this situation intracellular pH was sensitive to Na+ removal or amiloride addition, intracellular pH decreasing from 7.00 +/- 0.07 to 6.48 +/- 0.10 (p less than 0.01, N = 6) and from 6.86 +/- 0.06 to 6.32 +/- 0.01 (p less than 0.01, N = 7), respectively, in 15 min. The data suggest that in gastric epithelium exposed to luminal acid, physiological intracellular pH is primarily maintained by the buffer action of serosal HCO3- transported to the epithelial surface to impede the entry of luminal H+ into mucosal tissue. Removal of the sheltering HCO3- unmasks a second line, Na(+)-dependent and amiloride-sensitive intracellular pH regulatory mechanism, presumably a Na+/H+ antiport.

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

PubMed1991

Exogenous surface-active phospholipid protects Necturus gastric mucosa against luminal acid and barrier-breaking agents.

The nature of the protective action of exogenous surface-active phospholipid on gastric mucosa was studied in isolated Necturus antral mucosa by measuring intracellular pH and intraepithelial potentials and resistances with a microelectrode technique. Exposure of the antral mucosa to luminal pH 2 acidified intracellular pH in surface epithelial cells by 0.6-0.3 pH units. A 20-minute pretreatment with exogenous (pulmonary) surfactanlike phospholipid completely abolished this effect. Obviously, phospholipid protected the mucosa against intracellular acidosis by decreasing the apical cell membrane conductance to H+ (and other ions), because it increased apical cell membrane resistance by +108% and total transcellular resistance by +86% but had no significant effects on paracellular or total transepithelial resistances. In mucosas exposed to three barrier-breaking agents, 10 mmol/L acetylsalicylic acid, 20% (vol/vol) ethanol, and 10 mmol/L taurocholate, at acid luminal perfusate (pH 2.0-2.5), a profound intracellular acidification of 0.9-1.3 pH units/15 min occurred. Pretreatment of the tissue with phospholipid significantly opposed intracellular acidification, but the modulatory influences on the changes in intraepithelial potentials or resistances were less conspicuous and mostly insignificant.

Animals↗

PubMed1992

Intracellular pH in isolated Necturus duodenal mucosa exposed to luminal acid.

Regulation of intracellular pH (pHi) and its maintenance within physiological ranges during exposure to luminal acid was studied in isolated Necturus duodenal mucosa using liquid sensor microelectrodes. Exposure of the mucosa to luminal pH 2.7 caused significant intraepithelial acidification. Subsequent removal of HCO3-/CO2 (HEPES/O2 substitution) from the serosal perfusate caused a further decrease of pHi. Blocking of HCO3- transport across the basolateral cell membrane by addition of 4-acetamido-4,isothiosyanostilbene-2,2-disulfonic acid (SITS) to serosal perfusate also caused a slight but significant decrease of pHi. Removal of Na+ (choline substitution) from the serosal perfusate during acid exposure likewise caused a significant decrease in pHi, as did serosal addition of an inhibitor of Na+/H+ antiport, 1 mmol/L amiloride. When Na+ was removed from the serosal perfusate after HCO3- removal, pHi first rapidly acidified; this was followed after an initial 5-minute steady state by an uncontrolled progressive acidification at a rate of 0.33 pH unit/15 min without any further steady state. A similar but weaker effect could also be shown with amiloride addition. The epithelial surface pH was 7.13 +/- 0.08 at the apex of mucosal villus and 7.42 +/- 0.11 (n = 5) in the cryptal area between the villi, i.e., greater than 1 pH unit higher than that of the luminal bulk solution (pH 6), thus suggesting active alkalization of the epithelial surface. Removal of serosal HCO3-/CO2 decreased surface pH significantly both at the villus apex and at the cryptal area, suggesting that the surface alkalization is mediated by transport of serosal HCO3- to the epithelial surface. The data suggest that pHi in acid-exposed duodenal mucosa is primarily maintained within physiological range by an HCO3(-)-dependent mechanism, which, at least in part, exerts its action extracellularly by forming an alkaline buffer layer at the epithelial surface. If adequate serosal (or systemic) HCO3- is not available, a second-line Na(+)-dependent and amiloride-sensitive pHi-regulatory mechanism, presumably an Na+/H+ antiport, becomes the main regulator of pHi.

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

PubMed1992

Effects of aspirin on pathways of ion permeation in Necturus antrum: role of nutrient HCO3.

Intracellular microelectrodes were used to evaluate electrical properties of the cell membranes in Necturus antral mucosa during exposure to luminal acid alone (pH 4) or to 5 mmol/L aspirin [acetylsalicylic acid (ASA)] in the presence of luminal acid. When nutrient solutions were buffered by HCO3- (pH 7.3), ASA moderately depolarized and increased the resistances of both cell membranes. When nutrient solutions were buffered by HEPES (pH 7.3), ASA induced even greater depolarizations of the cell membranes. In addition, resistance of the apical membrane did not increase and resistance of the basolateral membrane decreased. The changes in basolateral membrane resistance were observed when tissues were exposed to 5 mmol/L salicylate but not during exposure to luminal acid alone or to acidified luminal solutions containing 5 mmol/L acetate, a small and permeable organic acid. Electron microscopy confirmed that these initial electrophysiological changes precede alterations in cell morphology. The findings suggest that nutrient HCO3- attenuates changes in membrane potentials caused by ASA. Loss of nutrient HCO3- seems to accelerate alterations in basolateral membrane resistance caused by ASA and its salicylate moiety.

Acetates↗

PubMed1995

Regulation of intracellular pH in isolated Necturus gastric mucosa during short-term exposure to luminal acid.

BACKGROUND/AIMS: Continuous exposure to gastric acid implies efficient control mechanisms of intracellular pH (pHi) in the gastric epithelium. This study assessed the roles of Na+, H+, and HCO3- transport mechanisms in controlling pHi during short-term exposure of the gastric epithelium to luminal acid. METHODS: pHi and Na+ activity (aiNa) were measured with liquid sensor microelectrodes in isolated Necturus antral mucosa, modulating ion transport mechanisms by ion removal and pharmacological inhibition. RESULTS: Short-term exposure to luminal acid (pH 2.3) acidified pHi by 0.3 pH units, whereafter pHi stabilized. This was associated with transient increase in aiNa. Blocking of Na+/H+ exchange (in the presence of HCO3-/CO2) by removal of Na+ or addition of amiloride eliminated the increase in aiNa and resulted in uncontrolled acidification of pHi. Similarly, blocking of HCO3- transport (in the presence of Na+) by removal of HCO3-/CO2 or addition of 4-acetamido-4-isothiocyanatostilbene-2,2-disulfonic acid resulted in uncontrolled acidification of pHi despite increase in aiNa. Blocking of Na+/K+ exchange with ouabain eliminated the recovery of aiNa and also resulted in uncontrolled acidification of pHi. CONCLUSIONS: The data indicate that during short-term exposure of the gastric mucosa to luminal acid, both Na+/H+ antiport and HCO3- transport are needed to control pHi and maintain it within physiological ranges.

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