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PubMed1994

Mechanisms of oxalate absorption and secretion across the rabbit distal colon.

To further evaluate the mechanisms of oxalate (Ox2-) transport in the intestine the following studies were performed using isolated, short-circuited segments of the rabbit distal colon (DC). In control buffer, the DC absorbed Ox2- (net Ox2- flux, JNetOx = 5.4 +/- 0.7 pmol.cm-1.h-1). Replacement of Na+ with N-methyl-D-glucamine (NMDG+) abolished Ox2- absorption by decreasing mucosal to serosal Ox2- flux (JmsOx), without affecting Cl- transport, while gluconate substitution for Cl- did not affect JNetOx or net Na+ flux (JNetNa). Addition of Na+ to the serosal side of tissues bathed by NMDG+ buffer increased JmsOx 40% without altering mucosal to serosal Cl- flux (JmsCl). Serosal amiloride or dimethyl amiloride (10(-3) M) abolished JNetOx by decreasing JmsOx, it increased serosal to muscosal Cl- flux (JsmCl) and it gradually inhibited short-circuit current (Isc). Mucosal amiloride (10(-4) M) abolished Ise but had no effect on Ox2- or Cl- fluxes. Serosal 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 10(-6) M) reduced JmsOx by 20% and JNetOx by 43% without affecting JmsCl or JNetCl. Dibutyryl cyclic adenosine monophosphate (dB-cAMP, 5 x 10(-4) M, both sides) stimulated Ox2- secretion (JNetOx = -12.6 +/- 3.3 pmol.cm-2.h-1). The dB-cAMP-induced secretion of Ox2- and Cl- were fully abolished by serosal furosemide (10(-4) M) and partially inhibited (35%) by 5 x 10(-4) M mucosal NPPB [5-nitro-2-(3-phenylpropylamino)-benzoic acid], a putative Cl- channel blocker.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1986

Current-noise analysis of the basolateral route for K+ ions across a K+-secreting insect midgut epithelium (Manduca sexta).

The isolated midgut of a lepidopteran larva (Manduca sexta), 5th instar was investigated with voltage-clamp and fluctuation analysis techniques. With high K+ insect saline on both sides the outward-directed short-circuit current (Isc) was carried by K+ (IK) from serosal to mucosal compartment. IK could be blocked, in a dose-dependent manner by serosal Ba2+ ions. There was no current with serosal Na+. Noise analysis of IK revealed a Lorentzian component in the power spectrum when Ba2+ was present in the serosal solution. The Ba2+/receptor kinetics show pseudo-first order characteristics only at low [Ba2+]s. For [Ba2+]s greater than KBa, the apparent Ba2+ association rate decreases with a hyperbolic course as a function of serosal [Ba2+] which could indicate some "substrate-inhibition"-like interaction of Ba2+ at its receptor site. It is concluded that the serosal membranes of the K+-secreting intestinal cells contain the common type of Ba2+-blockable K+ channel which provides the serosal pathway for K+ during secretion which is ultimately driven by the mucosally-located electrogenic K+-ATPase.

Animals↗

PubMed1999

Evidence for a Na+/Ca2+ exchange mechanism in frog skin epithelium.

In the present study we investigated the possible existence of a Na+/Ca2+ exchange mechanism in the basolateral membrane of the frog skin epithelium and whether such a mechanism plays a role in the regulation of transepithelial Na+ transport. Cytosolic calcium ([Ca2+]i) was measured with the probe fura-2 in a set-up in which pieces of tissue were mounted on the stage of an epifluorescence microscope. Na+ transport was measured as the amiloride-sensitive short-circuit current (Isc) using a conventional voltage clamp. Basal [Ca2+]i was 65+/-6 nM (n=15). Removal of Na+ from the mucosal solution had no effect on [Ca2+]i. When Na+ was removed from the serosal solution, [Ca2+]i increased biphasically to a peak of 220+/-38 nM (n=8, P=0.006). Readdition of Na+ to the serosal solution returned [Ca2+]i to control level. The serosal Na+ gradient and changes in [Ca2+]i were closely correlated; stepwise changes in serosal Na+ were followed by stepwise changes in [Ca2+]i. These observations indicate the existence of a Na+/Ca2+ exchange mechanism in the basolateral membrane of the frog skin epithelium. The transepithelial Na+ transport decreased from 13.2+/-1.8 to 9.2+/-1.5 microA cm-2 (n=8, P=0.049) when Na+ was omitted from the serosal solution. When this protocol was repeated in the absence of serosal Ca2+, Na+ transport decreased similarly from 16.7+/-1.7 to 11.6 +/-1. 8 microA cm-2 (n=6, P=0.004). We conclude that it is unlikely that the observed decrease in Isc after removal of serosal Na+ is due to an increase in [Ca2+]i per se.

Algorithms↗

PubMed1984

Feedback inhibition of sodium uptake in K+-depolarized toad urinary bladders.

Ouabain-blocked toad urinary bladders were maintained in Na+-free mucosal solutions, and a depolarizing solution of high K+ activity containing only 5 mM Na+ on the serosal side. Exposure to mucosal sodium (20 mM activity) evoked a transient amiloride-blockable inward current, which decayed to near zero within one hour. The apical sodium conductance increased in the initial phase of the current decay and decreased in the second phase. The conductance decrease required Ca2+ to be present on the serosal side and was more rapid when the mucosal Na+ activity was higher. At 20 mM mucosal Na+ and 3 mM serosal Ca2+ the initial (maximal) rate of inhibition amounted to 20% in 10 min. The conductance decrease could be accelerated by raising the serosal Ca2+ activity to 10 mM. The inhibition reversed on lowering the serosal Ca2+ to 3 microM and, in addition, the mucosal Na+ to zero. Exposure of the mucosal surface to the ionophore nystatin abolished the Ca2+ sensitivity of the transcellular conductance, showing that the Ca2+-sensitive conductance resides in the apical membrane. The data imply that in the K+-depolarized epithelia, cellular Ca2+, taken up from the serosal medium by means of a Na+-Ca2+ antiport, cause feedback inhibition by blockage of apical Na+ channels. However, the rate of inhibition is small, such that this regulatory mechanism will have little effect at 1 mM serosal Ca2+ and less than 20 mM cellular Na+.

Animals↗

PubMed1993

Comparative study of active absorption by the intestine and disposition of anomers of sugar-conjugated compounds.

Active absorption in the intestine and metabolism of the beta- and alpha-anomers of the glucoside and galactoside of p-nitrophenol (p-NP) were studied to find a more suitable prodrug for poorly absorbed drugs. The everted sac technique was used to investigate the intestinal absorption of these glycosides at 250 microM from the mucosal to the serosal side in the rat jejunum. The absorption clearance of p-nitrophenyl alpha-D-glucopyranoside (p-NP alpha glc) (0.271 +/- 0.089 microL/min/cm, mean +/- SE, N = 8) was much lower than that of p-nitrophenyl beta-D-glucopyranoside (p-NP beta glc) (4.45 +/- 0.34 microL/min/cm, mean +/- SE, N = 4) which is actively absorbed by a glucose transport carrier [Mizuma et al., Biochem Pharmacol 43: 2037-2039, 1992]. However, the major constituent appearing on the serosal side was p-NP (aglycone) after absorption of pNP alpha glc, whereas it was p-NP beta glc itself after absorption of p-NP beta glc. The total amount transported to the serosal side after 20 min of p-NP alpha glc absorption, which was similar to that of p-NP beta glc, was significantly decreased in the absence of Na+, indicating the active absorption of p-NP alpha glc by a Na(+)-dependent glucose transport carrier. Perfusion with a mucosal solution of p-NP alpha glc showed that the p-NP concentration on the serosal side (15.8 +/- 1.56 microM, mean +/- SE, N = 3) was significantly (P < 0.05) higher than that on the mucosal side (5.84 +/- 1.24 microM, mean +/- SE, N = 3) at 20 min. This indicated that the p-NP appearing on the serosal side was derived not from absorption of p-NP but from hydrolysis of p-NP alpha glc through the intestinal membrane during absorption. On the other hand, after absorption of p-nitrophenyl beta-D-galactopyranoside (p-NP beta gal), which is actively absorbed by glucose transport carrier, p-NP beta gal itself appeared mostly on the serosal side. However, p-nitrophenyl alpha-D-galactopyranoside (p-NP alpha gal) absorption, which resulted in appearance on the serosal side, was not significantly decreased in the presence of 1 mM phloridzin or in the absence of Na+, indicating that the contribution of the glucose transport carrier to p-NP alpha gal absorption was minimal. The order of the Na(+)-dependent intestinal absorption was p-NP beta glc > p-NP alpha glc > p-NP beta gal > p-NP alpha gal.

Animals↗

PubMed1991

Acid-induced increase in electrical conductance of guinea pig duodenal mucosa in vitro. Temporary protection by combined effects of bicarbonate and prostaglandin E2.

Electrical conductance as a sensitive indicator of acid damage has been investigated in guinea pig duodenal mucosa using Ussing-chamber techniques. Reductions of luminal pH from 7.4 to 3.0, 2.3, or 2.0 caused concentration-dependent, progressive increases in conductance, accompanied (pH 2.0) by a continuous increase in hydrogen permeation as determined by pH-stat titration. Increases in conductance and hydrogen flux were related to base-line conductance, with higher values conditioning for a sooner onset and/or more marked elevation. Conductance increases were prevented by timely back titration. Recently, it has been shown that serosal HCO3 reduces conductance by actions dependent on prostaglandins and serosal Na and sensitive to loop diuretics. Here, serosal HCO3 delayed the onset of acid-induced conductance increase by approximately 8 minutes, an effect reduced by omission of serosal Na and during exposure to serosal furosemide (10(-3) mol/L). In the presence of serosal indomethacin (10(-4) mol/L) and HCO3, prostaglandin E2 (10(-6) mol/L serosal bath) delayed the conductance increase. Because HCO3 secretion is negligible in this model, these results indicate effects of HCO3/prostaglandin E2 beyond mere buffering of invading hydrogen. These results are consistent with intracellular actions that tighten the paracellular pathway against acid and thus provide temporary protection from acid injury. In agreement with this view, HCO3 also limited conductance increases after luminal alkalinization by a furosemide-sensitive action.

Animals↗

PubMed1992

A possible relationship between KCl symport and basolateral K(+)-conductance in Necturus gallbladder epithelial cells.

1. Apical membrane potential (Va), transepithelial potential (VT), fractional apical voltage ratio (FVa = delta Va/delta VT), tissue resistance (RT), and intracellular Cl- (aiCl) and K+ (aiK) activities were measured in isolated gallbladders maintained between oxygenated bicarbonate-free physiological media (23 degrees C, pH 7.2 or 8.2) in a divided chamber. The basolateral membrane potential (Vb) was calculated from the measured values of Va and VT. 2. Cl- removal from the serosal medium (which should accelerate coupled basolateral KCl exit) significantly depolarized Vb, decreased aiCl, decreased FVa, increased RT, and attenuated the depolarization of Vb (delta Vb) induced by high K+ added to the serosal side. These changes are consistent with a decrease in the K(+)-conductance of the basolateral membrane (gbK). 3. Addition of furosemide (an inhibitor of KCl cotransport) to the serosal medium induced significant increases in Vb, FVa, and high K(+)-induced delta Vb, indicating an increase in gbK. 4. In the presence of serosal furosemide, Cl- removal from the serosal medium did not significantly alter Vb, aiCl or delta Vb from their corresponding values when serosal Cl- was present. 5. Serosal furosemide had no significant effect on aiK and aiCl measured with double-barreled ion-selective microelectrodes. 6. These results suggest the possibility of a reciprocal relationship between gbK and the rate of basolateral KCl cotransport. This may contribute to the maintenance of aiK in gallbladder epithelial cells.

Animals↗

PubMed2002

Differential responsiveness of proximal and distal parts of isolated guinea pig trachea.

This study addressed the question whether proximal and distal guinea pig tracheal segments respond differently to contractile agents. Using a perfused trachea set-up, histamine, KCl or the cyclo-oxygenase inhibitor, indomethacin, could be administered selectively to the mucosa (at the inside) or the serosa (at the outside) of the tracheal segments. Proximal parts contracted significantly more (40-60%) than distal parts when 1 mM histamine was administered to the mucosal or serosal side or when KCl (50 mM) was added to the serosal side. When histamine was administered to the mucosal side of epithelium-denuded segments, the contractions were twice as high in proximal than in distal parts (3057 vs. 1526 mg). Inhibition of tracheal cyclo-oxygenase with indomethacin at the mucosal side increased proximal and distal reactivity to mucosally administered histamine to the same extent. Serosal administration of indomethacin, however, increased histamine reactivity only in proximal segments (from 2690 to 5180 mg). In the latter segments, subsequent administration of histamine to the serosal side further increased the contraction, while serosal histamine in the absence of serosal indomethacin produced a relaxation (net difference of 4672 mg). In conclusion, the higher intrinsic contractility of proximal tracheal segments is counteracted by serosal cyclo-oxygenase products.

Animals↗

PubMed2000

Responses of frog skin Na(+) and Cl(-) transport to guanylin.

A possible role for the peptide hormone guanylin was investigated in frog skin (Rana pipiens) epithelium. Sodium and chloride fluxes in response to this peptide were evaluated in Ussing-type chambers. Net and unidirectional Na(+) fluxes were measured by using (22)Na(+) and atomic absorption analysis of total [Na(+)], whereas net Cl(-) fluxes were measured by using electrometric titration for [Cl(-)]. Mucosal application of guanylin (0.5-2.0 micromol/l) caused marked increases in serosal to mucosal net flux and efflux of Na(+). Serosal application of guanylin over the same dose range caused similar large increases in net serosal to mucosal (S-->M) Na(+) and Cl(-) flux as well as Na(+) efflux. Responses of Na(+) influx were small and inconsistent. When frog skin was bathed on the serosal side with Cl(-)-free Ringer's solution mucosal application of guanylin stimulated large efflux and S-->M net fluxes of Na(+). Serosal treatment yielded large Na(+) effluxes and S-->M Na(+) and Cl(-) net fluxes. When frog skin serosal surfaces were bathed with Na(+)- free Ringer's solution mucosal guanylin treatment had no effect but serosal treatment produced large S-->M Cl(-) net fluxes.

Animals↗

PubMed2004

Structural signaling regulates inflammation-induced enhanced restitution and increased Mib-1 and Bax-indexes after superficial injury in isolated guinea pig gastric mucosa.

Several growth factors and cytokines are involved in regulation of the immediate repair of gastrointestinal mucosa, a process also called restitution. Few data exist on the effect of inflammation on this process using an explant model, where the folded basal lamina is included. The aim of the present study was to investigate the effect of simulated inflammation on restitution and on concomitant proliferation and apoptosis in isolated guinea pig gastric mucosa. Paired gastric mucosae were mounted in Ussing chambers (37 degrees C) and a superficial injury was induced (1.25 M NaCl/5 min) followed by a 4-hr restitution (pH 7.3-7.5). During perfusion, simulated inflammation was induced (with 0.5 or 5.0 ng/ml IL-1beta or with activated polymorphonuclear [PMN] cells). The PI (proliferative index) and AI (apoptotic index) are expressed as the number of Mib-1- or Bax-immunopositive cells per 300 foveolar cells, respectively. The mean recovery of electrophysiological resistance of tissues (R) after injury and exposure to serosal IL-1beta during restitution was 95.2 +/- 5.3% (mean +/- SD), whereas the value for control tissues was 89.6 +/- 6.9% (P = 0.016; N = 9). The mean recovery of R in tissues exposured to activated serosal PMN cells during restitution was 97.6 +/- 2.7%, whereas the value for unexposed control tissues was 93.8 +/- 2.9 (P = 0.004; N = 9). The enhancing effect of PMN cells was partially eliminated by serosal anti-ICAM, whereas serosal cytochalasin D abolished the process completely. The PI of tissues exposed to serosal PMN cells was 34.6 +/- 17.3, whereas the value for unexposed controls was 24.7 +/- 15.5 (P = 0.04; N = 5). The corresponding AI values were 17.0 +/- 2.8 and 12.0 +/- 5.7, respectively (NS; N = 4). Simulated inflammation either with serosal IL-1beta or with activated PMN cells enhances restitution and proliferation, whereas their effect on AI is only suggestive. Exogenous serosal anti-ICAM modulates restitution, whereas cytochalasin D abolishes it completely, suggesting that the structural signaling system including focal adhesions and cytoskeleton plays a significant role in the regulation of restitution.

Animals↗

PubMed2001

The serosa of Manduca sexta (Insecta, Lepidoptera): ontogeny, secretory activity, structural changes, and functional considerations.

In Manduca sexta, the blastoderm forms successively and becomes immediately cellularized as the cleavage energids reach the surface of the oocyte. Presumptive serosal cells are large and contain 2 or 4 large polyploid nuclei; presumptive embryonic cells are small and mononuclear. All parts of the blastoderm participate in the uptake and digestion of yolk material. About 10 h post-oviposition, the blastoderm breaks at the amnioserosal fold and the extraembryonic part closes above the germ band and constitutes the serosa (12 h post-oviposition, i.e. 10% development completed). At once, the serosa starts to secrete a cuticle consisting of an epi- and a lamellated endocuticle. Detachment of the serosal cuticle, 22h post-oviposition, is reminiscent of apolysis of larval cuticle. Thereafter, the serosa deposits a membranous structure, the serosal membrane. The sercretory process lasts from 23h to 44h post-oviposition. At first a fine granular layer, then an amorphous, spongy-like, fibrillar layer is secreted via microvilli. This persisting membrane is tough, rubbery and very elastic. It may serve to bolster the serosa during katatrepsis (48h post-oviposition) and later embryonic movements. After detachment of the serosal membrane, 44h post-oviposition, a distinct subcellular reorganization of the serosa takes place. The nuclei become still larger and more irregular. Uptake of yolk granules, but not of lipid droplets, ceases, although interaction of serosa and yolk cells are intense. Serosal cells include many mitochondria, large areas of rER, besides some sER, increasing amounts of lysosomal bodies and prominent Golgi complexes. Most conspicuous is the assembly of spindle-shaped, electron-lucent vesicles below the apical surface. These vesicles may contain metabolic products which are released into the peripheral space. The studies show that the serosa assumes changing functions during embryogenesis: digestion of yolk substances, synthesis of a serosal cuticle and a serosal membrane, which may have a protective function, and excretion.

Animals↗

PubMed1963

The electrical characteristics of active sodium transport in the toad bladder.

The mechanism responsible for active sodium transport in the urinary bladder of the toad appears to be located at the serosal boundary of the epithelial cell layer of the bladder. Studies of the potential step observed at the serosal boundary in the open-circuited state were undertaken in an attempt to define the factors responsible for its production. Glass micropipettes were used to measure the serosal potential step in bladders exposed on the serosal side to solutions of high potassium or of high potassium and low chloride concentration. Observed potentials exceed the maximum values which would have been expected if the serosal potential step were a potassium or chloride diffusion potential. Measurements of net cation flux exclude the possibility of a diffusion potential at this border due to the passive movement of any anionic species. The observed independence of transbladder potential and short-circuit current from the pH of the serosal medium over a wide range of pH makes it unlikely that the observed serosal potential step is a hydrogen ion diffusion potential. We conclude that the active sodium transport mechanism in toad bladder is "electrogenic."

Biological Transport, Active↗

PubMed1972

Membrane potentials of epithelial cells in rat small intestine.

1. Stripped sacs of rat jejunum in which the outer muscle layers had been removed were found to maintain substantial transport and electrical activities.2. Mucosal and serosal membrane potentials of epithelial cells of normal and stripped everted sacs of rat jejunum were recorded in vitro together with the transmural potential difference.3. The cell interior was negative relative to both serosal and mucosal fluids, the transmural potential being the sum of the two membrane potentials.4. Changes in the transmural potentials in the presence of actively transferred hexoses and amino acids were entirely due to variations in the serosal potential, the mucosal potential being unchanged.5. Serosal and transmural potential increases on the addition of galactose were consistent with Michaelis-Menten kinetics, giving apparent K(m) values of 14.9 and 14.1 mM respectively.6. Phlorrhizin, ouabain, 2,4-dinitrophenol and sodium fluoroacetate inhibited serosal potential changes in the presence of galactose.7. Osmotic potentials resulting from transmural osmotic gradients originated from the serosal layers of the tissue.8. The results are consistent with the concept of a serosally located, electrogenic sodium pump which is stimulated by actively transferred hexoses and amino acids. The sodium-dependent entry mechanism at the mucosal membrane is non-electrogenic.

Alanine↗

PubMed1985

The secretory action of barium chloride in rat colon.

BaCl2, applied serosally, caused a rise in the p.d. and short-circuit current (s.c.c), and a decrease in tissue resistance in stripped sheets of rat colon. This response was dose dependent. Mucosal application of BaCl2 was without effect. The BaCl2-induced rise in s.c.c. was inhibited by reducing the serosal Na+ concentration to 25 mM. Lowering the mucosal Na+ concentration was without effect. Ouabain (10(-3) M in serosal fluid) and furosemide (10(-3) M in serosal fluid) both reduced the rise in s.c.c. induced by BaCl2. Flux determinations indicated that BaCl2 inhibited Na+ absorption and stimulated Cl- secretion by the colon. In vivo, BaCl2 increased fluid accumulation within the colonic lumen, an effect that was associated with a rise in the transcolonic p.d. Increasing the serosal K+ concentration to 20 mM reduced the responses to BaCl2, acetylcholine and theophylline, and this could not be entirely accounted for by the concomitant reduction in the serosal Na+ concentration. As high serosal K+ did not mimic the secretory response it would appear that BaCl2 does not act by blocking K+ channels. The rise in s.c.c. induced by BaCl2 was not reduced by Ca2+-free conditions, but it was inhibited by 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) and trifluoperazine. BaCl2 did not alter cyclic AMP production by colonic scrapes. It is concluded that BaCl2 induces colonic secretion by the release of intracellular Ca2+, which then combines with calmodulin to activate the secretory process.

Action Potentials↗

PubMed1988

A submucosal mechanism for catecholamine-induced increases in fluid absorption in rabbit ileum in vitro.

1. The effects of clonidine and dopamine on water movements across the mucosal and serosal surfaces of rabbit ileum have been investigated using a high-resolution method for monitoring water flows in vitro. 2. Theophylline (10 mM) and carbamyl choline (10 microM) caused a reduction in fluid inflow across the mucosal surface and a smaller decrease in fluid outflow across the serosal surface. Addition of the alpha 2-adrenergic agonist clonidine or dopamine fully reversed the theophylline, or carbamyl choline-induced decrease in mucosal inflow in a dose-related manner. 3. The effects of clonidine on mucosal inflow are blocked by the alpha 2-adrenergic antagonist, yohimbine. Yohimbine was much less effective than pimozide or d-butaclamol in blocking the effect of dopamine on mucosal inflow. These findings support the view that there are separate alpha 2-adrenergic and dopaminergic receptors. 4. The hydraulic conductance (Lp) of the serosal surface was measured directly from the change in serosal exit flow following addition of 2 mosmol kg-1 of polyethylene glycol (molecular mass 20,000 Da) to the serosal bathing solution. Theophylline reduced the Lp by 35%. Clonidine (1 microM) added to theophylline-treated tissues increased the Lp by 66%. This effect was prevented by yohimbine (1 microM). 5. The effects of theophylline, clonidine and dopamine on the permeability of the mucosal and serosal surfaces of the tissue to [3H]mannitol were measured. These showed that theophylline increased the rate of labelled mannitol loss across the mucosal surface but reduced the mannitol permeability across the serosal surface. This latter effect was reversed by clonidine and dopamine. 6. Changes in transepithelial electrical potential difference (PD), short-circuit current and resistance were monitored. Theophylline caused a rapid increase in PD and short-circuit current and a slower increase in resistance. Clonidine (5 microM) reversed the effects on PD and resistance but was without significant effect on short-circuit current. The results suggest that a major component of secretagogue-induced reduction in fluid transport in vitro is due to mechanical changes in the submucosa, probably induced by modulation of neurotransmitter release within the tissue.

Animals↗

PubMed1989

Stimulation of chloride secretion by N-formyl-methionylleucylphenylalanine (FMLP) in rabbit ileal mucosa.

1. Formyl-methionyl peptides are potent neutrophil chemoattractants which may be involved in inflammatory responses in the intestine. Effects of formyl-methionylleucylphenylalanine (FMLP) on electrical properties and Cl- fluxes were examined with the Ussing chamber technique employing stripped segments of rabbit ileal mucosa. 2. Serosal but not mucosal addition of FMLP elicited a transient (peak effect within 2 min), concentration-dependent (maximal effect at 30 nM and half-maximal effect at 3 nM) increase in short-circuit current (Isc) which was not inhibited by pretreatment of the tissue with mepyramine (10 microM), tetrodotoxin (0.1 microM) or atropine (10 microM). The related peptides FMLP-benzylamide (FMLP-benz) and methionyl-leucylphenylalanine (MLP) produced concentration-dependent increases in Isc which were qualitatively similar to FMLP. The order of potencies of these peptides was FMLP-benz greater than FMLP greater than MLP. 3. The lack of an effect of mucosal FMLP (300 nM) on Isc does not appear to be due to metabolism since addition of an aliquot of this bathing solution to the serosal bathing solution of a naive tissue increased Isc as expected. Addition of FMLP (30 nM) to the serosal bathing solution of a tissue pre-stimulated with serosal FMLP (30 nM) failed to elicit a response. 4. The increase in Isc produced by FMLP (30 nM) was inhibited by removal of Ca2+ from the serosal bathing solution and by removal of Cl- from both bathing solutions. FMLP (30 nM) increased the serosal-to-mucosal flux of Cl- and decreased the transepithelial conductance (Gt). 5. The cyclo-oxygenase inhibitors indomethacin (1 microM), mefenamate (10 microM) or piroxicam (30 microM) added to both the serosal and mucosal bathing solutions inhibited the increase in Isc elicited by FMLP (30 nM). 6. Measurement of release of immunoreactive thromboxane B2, 6-keto-PGF1 alpha and PGE2 revealed that FMLP (30 nM) selectively increased PGE2 release by an indomethacin-sensitive pathway. 7. Thus, in addition to being potent chemoattractants, formyl-methionyl peptides stimulate electrogenic Cl- secretion and also increase prostaglandin production.

Animals↗

PubMed1989

Conductive pathways for HCO3- in basolateral membrane of salamander intestinal cells.

To understand the route of HCO3- exit across the basolateral membrane of Amphiuma small intestinal cells during active H+ secretion the influence of bath HCO3- on serosal membrane potential (Vs) was measured using conventional microelectrodes. The villus sheet preparation was used, which allowed direct access to the basal membrane for microelectrode impalement. When tissues were incubated in Cl(-)-free (SO2-4 based) medium, Vs averaged -85.8 mV. Elevation of serosal bath [HCO3-] at constant CO2 increased Vs; reduction of the [HCO3-] reduced Vs and increased the fractional resistance of the serosal membrane. When serosal bath HCO3- and CO2 were completely replaced, Vs was -44.8 mV. The serosal membrane was also depolarized on complete replacement of medium HCO3- and CO2 when bath pH was buffered with phosphate. 4,4'-Dinitro-2,2'-stilbene disulfonate (DNDS) and acetazolamide blocked the decline in Vs produced by lowering serosal medium [HCO3-]. Replacement of serosal Na+ reduced Vs 32.7 mV. DNDS blocked this response. It is concluded that a Na+-dependent, stilbene-sensitive HCO3- exit pathway resides in the basolateral membrane of the intestinal cells. Possibly there is also a parallel, conductive pathway for HCO3-.

Acetazolamide↗

PubMed1986

Active potassium secretion by rabbit proximal colon.

Fluxes of K from mucosa to serosa or serosa to mucosa have been examined in stripped preparations of rabbit proximal and distal colon in vitro under short-circuit conditions in Ussing chambers. Results from these studies demonstrate that steady-state radioisotopic fluxes of K are achieved after 90 min and remain constant for at least 2 h. Determination of the K concentration dependence of the serosal-to-mucosal K flux revealed that this flux contains both saturable and nonsaturable components. Addition of ouabain (0.1 mM) abolished the saturable component of the serosal-to-mucosal K flux. The mucosal-to-serosal K flux is a linear function of K concentration between 1 and 20 mM under basal conditions. In paired tissues, serosal-to-mucosal K flux is always greater than mucosal-to-serosal flux under basal conditions resulting in net K secretion. However, addition of barium (2 mM) to the mucosal or serosal bathing solution had no significant effect on either unidirectional or net K fluxes. In addition, mucosal bumetanide (0.1 mM) or removal of Cl from both bathing solutions had no significant effect on unidirectional or net K fluxes. In rabbit distal colon, Cl removal from the bathing solutions significantly reduced serosal-to-mucosal K flux, resulting in net K absorption. These results indicate that rabbit proximal colon like rabbit distal colon actively secretes K. However, unlike distal colon the proximal colon does not possess an active K uptake mechanism at the apical cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗