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  • Exocrine secretion  (14)
  • Cl− conductance  (11)
  • Colon  (9)
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  • 1
    Electronic Resource
    Electronic Resource
    Regulation of epithelial ion channels by the cystic fibrosis transmembrane conductance regulator (1996)
    Springer
    Journal of molecular medicine 74 (1996), S. 527-534 
    Details
    ISSN: 1432-1440
    Keywords: Cystic fibrosis ; Cl- channel ; K+ channel ; Na+ channel ; Respiratory tract ; Colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In most epithelia ion transport is tightly regulated. One major primary target of such regulation is the modulation of ion channels. The present brief review focuses on one specific example of ion channel regulation by the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR functions as a cAMP-regulated Cl- channel. Its defect leads to the variable clinical pictures of cystic fibrosis (CF), which today is understood as a primary defect of epithelial Cl- channels in a variety of tissues such as the respiratory tract, intestine, pancreas, skin, epididymis, fallopian tube, and others. Most recent findings suggest that CFTR also acts as a channel regulator. Three examples are discussed by which CFTR regulates other Cl- channels, K+ channels, and epithelial Na+ channels. From this perspective it is evident that CFTR may play a major role in the integration of cellular function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00204979
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  • 2
    Electronic Resource
    Electronic Resource
    Regulation of epithelial ion channels by the cystic fibrosis transmembrane conductance regulator (1996)
    Springer
    Journal of molecular medicine 74 (1996), S. 527-534 
    Details
    ISSN: 1432-1440
    Keywords: Key words Cystic fibrosis ; Cl ; channel ; K+ channel ; Na+ channel ; Respiratory tract ; Colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Abstract: In most epithelia ion transport is tightly regulated. One major primary target of such regulation is the modulation of ion channels. The present brief review focuses on one specific example of ion channel regulation by the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR functions as a cAMP-regulated Cl–channel. Its defect leads to the variable clinical pictures of cystic fibrosis (CF), which today is understood as a primary defect of epithelial Cl–channels in a variety of tissues such as the respiratory tract, intestine, pancreas, skin, epididymis, fallopian tube, and others. Most recent findings suggest that CFTR also acts as a channel regulator. Three examples are discussed by which CFTR regulates other Cl–channels, K+ channels, and epithelial Na+ channels. From this perspective it is evident that CFTR may play a major role in the integration of cellular function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001090050056
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  • 3
    Electronic Resource
    Electronic Resource
    Characterization of human sweat duct chloride conductance by chloride channel blockers (1987)
    Springer
    Pflügers Archiv 408 (1987), S. 511-514 
    Details
    ISSN: 1432-2013
    Keywords: Human sweat duct ; Cl− conductance ; Cl− channel blockers ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To characterize the chloride conductance of human sweat duct the effect of various analogues of diphenylamine-2-carboxylate was investigated on the transepithelial potential difference (PDT) and resistance (R T ) of isolated microperfused sweat ducts. Although the most powerful analogues which block Cl− channels in various secretory and absorptive epithelia were ineffective, a number of analogues (in particular Cl substituted ones) were found which at high concentrations significantly and reversibly increased PDT andR T . The data suggest that the main chloride conductance pathway of sweat duct epithelium resides in the cell membranes rather than in the tight junctions. In addition the different blocking spectra of the chloride conductances of sweat duct and tracheal epithelium (Welsh MJ, Science 232:1648, 1986) suggest that the combined impairment of both conductances in cystic fibrosis does not result from a molecular defect in the Cl− channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585077
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  • 4
    Electronic Resource
    Electronic Resource
    Properties of the luminal membrane of isolated perfused rat pancreatic ducts (1988)
    Springer
    Pflügers Archiv 411 (1988), S. 546-553 
    Details
    ISSN: 1432-2013
    Keywords: Pancreas ; Isolated perfused ducts ; Luminal membrane ; Cl− conductance ; Cl−/HCO 3 − antiport ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to investigate by what transport mechanism does HCO 3 − cross the luminal membrane of pancreatic duct cells, and how do the cells respond to stimulation with dibytyryl cyclic AMP (db-cAMP). For this purpose a newly developed preparation of isolated and perfused intra-and interlobular ducts of rat pancreas was used. Responses of the epithelium to inhibitors and agonists were monitored by electrophysiological techniques. Addition of HCO 3 − /CO2 to the bath side of nonstimulated ducts depolarized the PD across the basolateral membrane (PDbl) by about 9mV, as also observed in a previous study [21]. This HCO 3 − effect was abolished by Cl− channel blockers or SITS infused into the lumen of the duct: i. e. 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB, 10−5 M) hyperpolarized PDbl by 8.2±1.6 mV (n=13); 3′,5-dichlorodiphenylamine-2-carboxylic acid (DCl-DPC, 10−5 M) hyperpolarized PDbl by 10.3±1.7 mV (n=10); and SITS hyperpolarized PDbl by 7.8±0.9 mV (n=4). Stimulation of the ducts with dbcAMP in the presence of bath HCO 3 − /CO2 resulted in depolarization of PDbl, the ductal lumen became more negative and the fractional resistance of the luminal membrane decreased. Together with forskolin (10−6 M), db-cAMP (10−4 M) caused a fast depolarization of PDbl by 33.8±2.5 mV (n=6). When db-cAMP (5×10−4 M) was given alone in the presence of bath HCO 3 − /CO2, PDbl depolarized by 25.3±4.2 mV (n=10). In the absence of exogenous HCO 3 − , db-cAMP also depolarized PDbl by 24.7±3.0 mV (n=10). The present data suggest that in the luminal membrane of pancreatic duct cells there is a Cl− conductance in parallel with a Cl−/HCO 3 − antiport. Dibutyryl cyclic AMP increases the Cl− conductance of the luminal membrane. Taking together our present results, and the recent data obtained for the basolateral membrane [21], a tentative model for pancreatic HCO 3 − transport is proposed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582376
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  • 5
    Electronic Resource
    Electronic Resource
    The ion conductances of colonic crypts from dexamethasone-treated rats (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 419-426 
    Details
    ISSN: 1432-2013
    Keywords: Colon ; Triamterene ; Amiloride ; Na+ channel ; Cl− channel ; K+ channel ; Carbachol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole-cell patch-clamp studies were performed in isolated colonic crypts of rats pretreated with dexamethasone (6 mg/kg subcutaneously on 3 days consecutively prior to the experiment). The cells were divided into three categories according to their position along the crypt axis: surface cells (s.c.); mid-crypt cells (m.c.) and crypt base cells (b.c.). The zero-current membrane voltage (V m) was −56 ± 2 mV in s.c (n = 34); −76 ± 2 mV in M.C. (n = 47); and −87 ± 1 mV in b.c. (n = 87). The whole-cell conductance (G m) was similar (8–12 nS) in all three types of cells. A fractional K+ conductance accounting for 29–67% ofG m was present in all cell types. A Na+conductance was demonstrable in s.c. by the hyperpolarizing effect onV m of a low-Na+ (5 mmol/1) solution. In m.c. and b.c. the hyperpolarizing effect was much smaller, albeit significant. Amiloride had a concentration-dependent hyperpolarizing effect onV m in m.c. and even more so in s.c.. It reducedG m by approximately 12%. The dissociation constant (K D) was around 0.2 μmol/l. Triamterene had a comparable but not additive effect (K D = 30 μmol/l,n = 14). Forskolin (10 μmol/l, in order to enhance cytosolic adenosine 3′, 5′-cyclic monophosphate or CAMP) depolarizedV m in all three types of cells. The strongest effect was seen in b. c..G m was enhanced significantly in b.c. by 83% (forskolin) to 121% [8-(4-chlorophenylthio)cAMP]. The depolarization ofV m and increase inG m was caused to large extent by an increase in Cl− conductance as shown by the effect of a reduction in bath Cl− concentration from 145 to 32 mmol/1. This manocuvre hyperpolarizedV m under control conditions significantly by 6–9 mV in all three types of cells, whilst it depolarizedV m in the presence of forskolin in m.c. and in b.c.. These data indicate that s.c. of dexamethasone-treated rats possess mostly a K+ conductance and an amiloride- and Tramterene-inhibitable Na+ conductance. m.c. and b.c. possess little or no Na+ conductance; theirV m is largely determined by a K+ conductance. Forskolin (via cAMP) augments the Cl− conductance of m.c. and b.c. but has only a slight effect on s.c.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207281
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  • 6
    Electronic Resource
    Electronic Resource
    Chloride channels in the luminal membrane of rat pancreatic acini (1997)
    Springer
    Pflügers Archiv 434 (1997), S. 188-194 
    Details
    ISSN: 1432-2013
    Keywords: Key words Exocrine pancreas ; Cl ; channel ; Cl ; secretion ; Exocrine secretion ; Patch clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Pancreatic acini secrete Na+, Cl–and H2O in response to secretagogues such as acetylcholine. Cl–channels in the luminal membrane are a prerequisite for this secretion. The properties of the corresponding conductance have previously been examined using whole-cell recordings. The present study attempts to examine the properties of the single channels in cell-attached and cell-free excised patches from the luminal membrane. To this end the pipettes were filled with an N-methyl-D-glucamine (NMDG+) chloride/gluconate solution. The voltage-clamp range was chosen to be pipette positive (cell negative, –60 to –130 mV) in order to increase the driving force for outward Cl–currents. Under resting conditions cell attached luminal patches had very few single-channel currents (12 out of 45 experiments). Their incidence was sharply increased by carbachol (CCH, 1 μmol/l) in 41 out of 45 experiments. The single-channel conductance of these channels was 1.97 ± 0.05 pS. The properties of these channels in excised patches were examined further: their single-channel conductance was 2.2 ± 0.07 pS (n = 59) and their conductance selectivity was I– 〉 Br– 〉 Cl– 〉〉 gluconate. None of the typical Cl–channel blockers (DIDS, NPPB, glibenclamide 100 μmol/l) blocked these channels. It is concluded that the luminal membrane of the rat pancreatic acinus possesses Cl–channels with very low conductance which are activated by carbachol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050382
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  • 7
    Electronic Resource
    Electronic Resource
    Transmitter-induced changes of the membrane voltage of HT29 cells (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 224-229 
    Details
    ISSN: 1432-2013
    Keywords: Cl− conductance ; HT29 ; P2 receptor ; Colon ; Cl− secretion ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The colonic carcinoma cell line HT29 was used to examine the influence of agonists increasing cytosolic cAMP and Ca2+ activity on the conductances and the cell membrane voltage (V m). HT29 cells were grown on glass cover-slips. Cells were impaled by microelectrodes 4–10 days after seeding, when they had formed large plaques. In 181 impalements V m was −51±1 mV. An increase in bath K+ concentration from 3.6 mmol/l to 18.6 mmol/l or 0.5 mmol/l Ba2+ depolarized the cells by 10±1 mV (n=49) or by 9±2 mV (n=3), respectively. A decrease of bath Cl− concentration from 145 to 30 mmol/l depolarized the cells by 11±1 mV (n=24). Agents increasing intracellular cAMP such as isobutylmethylxanthine (0.1 mmol/l), forskolin (10 μmol/l) or isoprenaline (10 μmol/l) depolarized the cells by 6±1 (n=13), 15±3 (n=5) and 6±2 (n=3) mV, respectively. In hypoosmolar solutions (225 mosmol/l) cells depolarized by 9±1 mV (n=6). Purine and pyrimidine nucleotides depolarized the cells dose-dependently with the following potency sequence: UTP 〉 ATP 〉 ITP 〉 GTP 〉 TIP 〉 CTP = 0. The depolarization by ATP was stronger than that by ADP and adenosine. The muscarinic agonist carbachol led to a sustained depolarization by 27±6 mV (n=5) at 0.1 mmol/l, and to a transient depolarization by 12±4 mV (n=5) at 10 μmol/l. Neurotensin depolarized with a half-maximal effect at around 5 nmol/l. The depolarization induced by nucleotides and neurotensin was transient and followed by a hyperpolarization. We confirm that HT29 cells possess Cl−- and K+-conductive pathways. The Cl− conductance is regulated by intracellular cAMP level, cytosolic Ca2+ activity, and cell swelling. The K+ conductance in HT29 cells is regulated by intracellular Ca2+ activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374831
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  • 8
    Electronic Resource
    Electronic Resource
    Increase in cytosolic Ca2+ regulates exocytosis and Cl− conductance in HT29 cells (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 329-334 
    Details
    ISSN: 1432-2013
    Keywords: Exocytosis ; Membrane capacitance ; Cl− channel ; Cl− secretion ; Colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Increases of cytosolic Ca2+, as occur with agonists such as ATP, neurotensin (NT), hypotonic cell swelling and ionomycin, enhance the membrane conductance (G M) and hence the input conductance (G I) of HT29 cells. In the present study we have examined whether these increases in G M are paralleled by exocytosis. To this end the membrane capacitance (C M) of HT29 cells was measured by patch clamp techniques. Two methods to monitor C M were used: a direct method (DM) and a phase tracking method (PTM). With the DM the following results were obtained. NT (10−8 mol/l, n=9) increased G M and C m significantly from 2.4±0.3 nS and 23.5±3 pF to 32±8 nS and 27.3±3.1 pF respectively. ATP (10−4 mol/l, n=29) had a very similar effect. G m and C m were increased from 5.7±1 nS and 36±4.4 pF to 111±21 nS and 44±5.4 pF respectively. Hypotonic cell swelling (160 mosmol/l, n=18) had a comparable effect: G M and C M were increased from 4.9±1 nS and 30±4.1 pF to 46±10 nS and 37±4.9 pF respectively. Ionomycin (10−7 mol/l, n=4) gave similar results. With the PTM it was possible to monitor the rapid changes in G M and C M, as they were induced by ATP (n=42) and NT (n=29), with high time resolution. The transient and instantaneous (〈 1 s) increases in G I (from 2.1±0.4 to 21.7±1.7 nS in the case of ATP, and from 2.3±0.4 to 26.6±3.1 nS in the case of NT) were closely paralleled by transient increases in C m (from 17.6±1.4 to 21.1±1.7 pF in the case of ATP, and from 20.6±2.3 to 24.3±2.6 pF in the case of NT). The present data indicate that transient (ATP, NT) or more stable (hypotonic cell swelling, ionomycin) increases in [Ca2+]i produce corresponding increments in G m and C M. The relative changes in both parameters correlate with each other. These findings are compatible with the view that exocytosis is related to the Ca2+-mediated control of Cl− conductance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00384360
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  • 9
    Electronic Resource
    Electronic Resource
    Regulation of the Na+2Cl–K+ cotransporter in in vitro perfused rectal gland tubules of Squalus acanthias (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 521-528 
    Details
    ISSN: 1432-2013
    Keywords: Key words cAMP ; Cl ; channels ; Cl ; secretion ; Exocrine secretion ; K+ channels ; Volume regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Previously it has been shown that the Na+2Cl–K+ cotransporter accepts NH4 + at its K+ binding site. This property can be used to estimate its transport rates by adding NH4 + to the bath and measuring the initial furosemide-dependent rates of change in BCECF fluorescence. We have utilized this technique to determine the regulation of the furosemide-inhibitable Na+2Cl–K+ cotransporter in in vitroperfused rectal gland tubules (RGT) of Squalus acanthias. Addition of NH4 + to the bath (20 mmol/l) led to an initial alkalinization, corresponding to NH3 uptake. This was followed by an acidification, corresponding to NH4 + uptake. The rate of this uptake was quantified by exponential curve fitting and is given in arbitrary units (Δfluorescence/time). This acidification could be completely inhibited by furosemide. In the absence of any secretagogue preincubation of RGT in a low Cl– solution (6 mmol/l, low Cl–) for 10 min enhanced the uptake rate significantly from 4.04±0.51 to 12.7±1.30 (n=5). The addition of urea (200 mmol/l) was without effect, but the addition of 300 mmol/l mannitol (+300 mannitol) enhanced the rate significantly from 7.24±1.33 to 14.7±4.6 (n=6). Stimulation of NaCl secretion by a solution maximizing the cytosolic cAMP concentration (Stim) led to a significant increase in NH4 + uptake rate from 5.00±1.33 to 13.3±1.54 (n=6). Similar results were obtained in the additional presence of Ba2+ (1 mmol/l): the uptake rate was increased significantly from 4.23±0.34 to 15.1±1.86 (n=16). In the presence of Stim low Cl– had no additional effect on the uptake rate: 15.1±3.1 versus 15.2±2.8 in high Cl– (n=6). The uptake rate in Stim containing additional +300 mannitol (22.3±4.0, n=5) was not significantly different from that obtained with Stim or +300 mannitol alone. By whatever mechanism the NH4 + uptake rate was increased furosemide (500 µmol/l) always reduced this rate to control values. Hence three manoeuvres enhanced furosemide-inhibitable uptake rates of the Na+2Cl–K+ cotransporter probably independently: (1) lowering of cytosolic Cl– concentration; (2) cell shrinkage; and (3) activation by cAMP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050667
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  • 10
    Electronic Resource
    Electronic Resource
    Crypt base cells show forskolin-induced Cl− secretion but no cation inward conductance (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 427-434 
    Details
    ISSN: 1432-2013
    Keywords: Key words Colon ; Loop diuretics ; Na+ channel ; Cl ; channel ; Non-selective channel ; Exocrine secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole-cell patch-clamp studies in base cells of isolated colonic crypts of rats pretreated with dexa-methasone were performed to examine the effects of stimulation by forskolin (10 μmol/l). The experiments were designed in order to distinguish between two postulated effector mechanisms: the activation of a non-selective cation channel and the activation of Cl− channels. As shown in an accompanying report, forskolin depolarizes the membrane voltage (V m) by some 40–50 mV and enhances the whole-cell membrane conductance (G m) substantially in these cells. In this report all experiments were performed in the presence of forskolin. A reduction of the bath Na+ concentration from 145 to 2 mmol/l led to a hyperpolarization of V m by some 20–30 mV. This hyperpolarization occurred very slowly suggesting that the hyperpolarization produced by the low-Na+ solution was caused indirectly and not by a change in the equilibrium potential for Na+, E Na+. A complete kinetic analysis of the effect on voltage of bath Na+ revealed a saturation-type relation with a high apparent affinity for Na+ of around 5–10 mmol/l. A reduction in bath Cl− concentration from 145 to 32 mmol/l caused a depolarization of V m from −34 ± 3 to −20 ± 4 mV (n = 13) in the presence of a high bath Na+ concentration, but had the opposite effect at low (5 mmol/l) Na+ concentrations: V m was hyperpolarized from −46 ± 4 to −62 ± 6 mV (n = 13). If the effect of Na+ on V m was caused by a non-selective cation channel the opposite would have been expected. To test directly whether the Na+2Cl−K+ cotransporter was responsible for the effects of changes in bath Na+ on V m, the effects of increasing concentrations of several loop diuretics were examined. Furosemide, piretanide, torasemide and bumetanide (up to 0.1–0.5 mmol/l) all hyperpolarized V m, albeit only by less than 10 mV. Another subclass of loop diuretics containing a tetrazolate in position 1 [e.g. azosemide, no. 19A and no. 20A from Schlatter E, Greger R, Weidtke C (1983) Pflüger Arch 396: 210–217] were much more effective. Azosemide hyperpolarized V m from −46 ± 3 to −74 ± 2 mV (n = 18) and reduced G m from 11 ± 1 to 4 ± 1 nS (n = 14). These data indicate that forskolin stimulates Cl− secretion in these cells by a mechanism fully compatible with the current scheme for exocrine secretion involving the Na+2Cl−K+ cotransporter.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207282
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