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  • HT29  (14)
  • Cl− secretion  (8)
  • Cystic fibrosis  (8)
  • Rat  (7)
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  • 11
    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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  • 12
    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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  • 13
    Electronic Resource
    Electronic Resource
    Evidence for agonist-induced export of intracellular Ca2+ in epithelial cells (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 423-430 
    Details
    ISSN: 1432-2013
    Keywords: [Ca2+]i export ; Thapsigargin ; fura-2 ; HT29 ; CFPAC-1 ; ATP ; Carbachol ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is increasing evidence that some agonists not only induce intracellular Ca2+ increases, due to store release and transmembranous influx, but also that they stimulate Ca2+ efflux. We have investigated the agonist-stimulated response on the intracellular Ca2+ activity ([Ca2+]i) in the presence of thapsigargin (10−8 mol/l, TG) in HT29 and CFPAC-1 cells. For CFPAC-1 the agonists ATP (10−7–10−3 mol/l, n=9), carbachol (10−6–10−3 mol/l, n=5) and neurotensin (10−10–10−7 mol/l, n=6) all induced a concentration-dependent decrease in [Ca2+]i in the presence of TG. Similar results were obtained with HT29 cells. This decrease of [Ca2+]i could be caused by a reduced Ca2+ influx, either due to a reduced driving force for Ca2+ in the presence of depolarizing agonists or due to agonist-regulated decrease in Ca2+ permeability. Using the fura-2 Mn2+ quenching technique we demonstrated that ATP did not slow the TG-induced Mn2+ quench. This indicates that the agonist-induced [Ca2+]i decrease in the presence of TG was not due to a reduced influx of Ca2+ into the cell, but rather due to stimulation of Ca2+ export. We used the cell attached nystatin patch clamp technique in CFPAC-1 cells to examine whether, in the presence of TG, the above agonists still led to the previously described electrical changes. The cells had a mean membrane voltage of −49±3.6 mV (n=9). Within the first 3 min ATP was still able to induce a depolarization which could be attributed to an increase in Cl− conductance. This was expected, since at this time after TG stimulation all Ca2+ agonists still liberated some [Ca2+]i. When TG incubation was prolonged, agonist application led to strongly attenuated or to no electrical responses. Therefore, the agonist-stimulated [Ca2+]i decrease cannot be explained by the reduction of the driving force for Ca2+ into the cell. In the same cells hypotonic swelling (160 mosmol/l, n=15) still induced a further [Ca2+]i increase in the presence of TG and concomitantly induced Cl− and K+ conductances. We conclude that the agonist-induced decrease of [Ca2+]i in the presence of TG probably unmasks a stimulation of [Ca2+]i export.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374904
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  • 14
    Electronic Resource
    Electronic Resource
    Small and intermediate conductance chloride channels in HT29 cells (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 456-464 
    Details
    ISSN: 1432-2013
    Keywords: Cl− channels ; Cl− secretion ; HT29 ; Ca2+ ; cAMP ; Protein kinase A ; Cytosolic inhibitor ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recently, it has been shown that intermediate conductance outwardly rectifying chloride channels (ICOR) are blocked by cytosolic inhibitor (C. I.) found in the cytosol of human placenta and epithelial cells. C. I. also reduced the baseline current in excised membrane patches of HT29 cells. In the present study, this effect of C. I. was characterized further. Heat treated human placental cytosol was extracted in organic solvents and dissolved in different electrolyte solutions. It is shown that the reduction of baseline conductance (g o) is caused by inhibition of small non-resolvable channels, which are impermeable to Na+ and SO4 2−, but permeable to Cl−. The regulation of these small Cl−-conducting channels (g o) and of ICOR was examined further. First, no activating effects of protein kinase A (PKA) on the open probability (P o) of the ICOR or on the go) were observed. The Po of the ICOR was reduced by 22% in a Ca2+-free solution. g o was insensitive to changes in the Ca2+ activity. The effects of C. I. from a cystic fibrosis (CF) placenta and the CF pancreatic duct cell line CFPAC-1 were compared with the effects of corresponding control cytosols, and no significant differences between CF and control cytosols were found. We conclude that the excised patches of HT29 cells contain ICOR and small non-resolvable Cl−-conducting channels which are similarly inhibited by C. I. Apart from a weak effect of Ca2+ on the ICOR, g o and the ICOR do not seem to be directly controlled by Ca2+ or PKA. C. I. of normal and CF epithelia have a similar inhibitory potency on Cl− channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374908
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  • 15
    Electronic Resource
    Electronic Resource
    The amiloride inhibitable Na+ conductance of rat colonic crypt cells is suppressed by forskolin (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 984-986 
    Details
    ISSN: 1432-2013
    Keywords: Cl− secretion ; Na+ absorption ; CAMP ; exocrine secretion ; Cl− channel ; Na+ channel ; colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previously we have shown that mid crypt cells of corticoid treated rats possess an amiloride inhibitable Na+ conductance (NAC) and show an increased Cl− conductance when stimulated by prostaglandin or the second messenger CAMP. The NAC is supposed to determine the magnitude of NaCl absorption. The Cl− conductance defines the magnitude of NaCl secretion. In the present whole cell (WC) patch clamp study we have examined whether the amiloride (3 μmol/l) inhibitable NAC is downregulated when the Cl− conductance is increased by forskolin (5 μmol/l, n = 20) or the phosphodiesterase inhibitor IBMX (1 mmol/l, n = 5). Under control conditions the amiloride inhibitable NAC was 2.7 ± 0.4 nS. Forskolin depolarized the voltage from -58 ± 2.0 to-48 ± 1.9 mV and enhanced the WC conductance by 3.25 ± 0.6 nS in these cells. The amiloride inhibitable NAC was reduced to 0.38 ± 0.2 nS. These data confirm that forskolin enhances the Cl− conductance in these cells and they show for the first time that the Na+ conductance is reduced simultaneously. Thus the cells are able to change the direction of NaCl transport from absorption to secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02332187
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  • 16
    Electronic Resource
    Electronic Resource
    cAMP stimulation of CFTR-expressing Xenopus oocytes activates a chromanol-inhibitable K+ conductance (1996)
    Springer
    Pflügers Archiv 432 (1996), S. 516-522 
    Details
    ISSN: 1432-2013
    Keywords: Key words Cl ; channel ; K+ channel ; Cellular homeostasis ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Cystic fibrosis transmembrane conductance regulator (CFTR) functions as a Cl–channel in a large variety of cells expressing this protein. Recently evidence has accumulated that it also regulates other ion channels. A coordinated increase in Cl–and K+ conductances is necessary in many Cl–-secreting epithelia. This has, for example, recently been demonstrated for the colonic crypt, for which a new type of K+ channel and a specific inhibitor of this channel, the chromanol 293B, have been described. In the present study we have examined whether the cAMP-evoked activation of CFTR, overexpressed in Xenopus oocytes, in addition to its known activation of a Cl–conductance, also upregulates endogenous K+ channels. It is shown that CFTR-cRNA-injected but not water-injected oocytes possess a cAMP-activated Cl–conductance. Of the cAMP-induced whole-cell current increase, 15–25% was due to a 293B-, Ba2+and TEA+-inhibitable K+ conductance. The cRNA of the mutated CFTR (ΔF508 CFTR) had no such effect. We conclude that cAMP activated CFTR and an endogenous IsK-type and 293B-sensitive K+ conductance. Similar events, occurring, for example, in the colonic crypt possessing CFTR and 293B-sensitive K+ channels, might explain the coordinated cAMP-mediated increase in Cl–and K+ conductances.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050164
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  • 17
    Electronic Resource
    Electronic Resource
    Bicarbonate permeability of epithelial chloride channels (1991)
    Springer
    Pflügers Archiv 417 (1991), S. 616-621 
    Details
    ISSN: 1432-2013
    Keywords: Bicarbonate permeability ; Bicarbonate conductance ; Cl− channels ; HT29 ; T84 ; Respiratory cells ; Bicarbonate channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bicarbonate permeability of epithelial chloride channels has been studied using the patch-clamp technique. The experiments were performed in excised insideout oriented membrane patches from three different cultured cell types: (a) HT29 colon carcinoma cell line, (b) T84 colon carcinoma cell line, and (c) respiratory epithelial cells (REC) in primary culture. In all three preparations we observed outwardly rectifying chloride channels with similar conductances with 145 mmol/l NaCl solution in the pipette and in the bath (Cl− pipette/ Cl− bath). When Cl− was replaced by HCO 3 − in the bath (Cl−/HCO 3 − ) the conductance of the channel at negative clamp voltages was reduced significantly by 40% for HT29 (n=6), 39% for T84 (n=7), and 38% for REC (n=6). Similarly, the zero-current potential (VI=0) was shifted from 0 mV (Cl−/Cl−) to negative values (Cl−/ HCO 3 − ) revealing permeability ratios $${{P_{{\text{Cl}}} } \mathord{\left/ {\vphantom {{P_{{\text{Cl}}} } {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}} \right. \kern-\nulldelimiterspace} {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}$$ of 2.4±0.1 for HT29 (n=6), 2.0±0.1 for T84 (n=7), and 1.8±0.1 for REC (n=7). With NaHCO3 as the pipette solution and NaCl in the bath, the VI=0 was positive and a $${{P_{{\text{Cl}}} } \mathord{\left/ {\vphantom {{P_{{\text{Cl}}} } {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}} \right. \kern-\nulldelimiterspace} {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}$$ , value of 2.3±0.1 was determined for HT29 (n=5). Replacement of Cl− in the bath by HCO 3 − reduced V I=0 to values close to 0 mV. In another series of experiments, the pipette was filled with 145 mmol/l NaCl and the bath contained 35 mmol/l NaCl to which 35 mmol/l NaHCO3 were added. We found that neither the conductance for the inward current nor VI=0 was changed significantly with the additon of NaHCO3 (HT29, n=6). We conclude that the HCO 3 − permeability and HCO 3 − conductance of these channels is about half of that for Cl−.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00372960
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  • 18
    Electronic Resource
    Electronic Resource
    Na+ and Cl− conductances in airway epithelial cells: increased Na+ conductance in cystic fibrosis (1995)
    Springer
    Pflügers Archiv 431 (1995), S. 1-9 
    Details
    ISSN: 1432-2013
    Keywords: Na+ channel ; Respiratory epithelial cells ; Human Na+ channel ; Micropuncture ; Patch clamp ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Na+ and Cl− conductances in the apical membrane of respiratory epithelial cells are essential for electrolyte and water transport in the airways. Apart from the well described defect in adenosine 3′∶5′ cyclic monophosphate-(cAMP-) dependent activation of Cl− conductances in cystic fibrosis (CF), an increased Na+ conductance has also been reported from transepithelial measurements. In the present experiments we tried to identify these conductances in nasal epithelial cells using patch-clamp and microelectrode techniques. With these methods we found identical and relatively low membrane voltages of about −36 mV in both freshly isolated and primary cultured normal and CF nasal epithelial cells. A Cl− conductance could be activated by cAMP in normal (ΔG=3.1±0.8 nS, n=10) but not in CF (ΔG=0.3±0.1 nS, n=11) cells, whereas Ca2+-dependent Cl− currents activated by adenosine 5′-triphosphate (ATP) and bradykinin were present in both types of cells. Cell-attached membrane patches from stimulated cells did not reveal discernible singlechannel events when activated with any of the agonists. A Na+ conductance was also detected in freshly isolated ciliated respiratory cells in impalement studies, as evidenced by the hyperpolarization induced by 10 μmol/l amiloride (ΔV= −5.2±0.6 mV, n=56) and when Na+ was replaced in the bath by N-methyld-glucamine (NMDG) (ΔV = −5.7±0.9 mV, n=14). In whole-cell patch-clamp experiments, the amilorideinduced hyperpolarization was significantly larger in CF (ΔV = −9.7±2.4 mV, n=22) when compared to normal (ΔV = −3.3±0.9 mV, n=27) cells in short-term culture. Reverse transcriptase polymerase chain reaction analysis of normal respiratory cells identified messenger RNA of both the cystic fibrosis transmembrane conductance regulator (CFTR) as well as the human epithelial Na+ channel (hNaCh). The present experiments confirm the absence of a cAMP-dependent Cl− conductance in CF respiratory epithelial cells and support previous findings obtained in transepithelial and microelectrode studies which indicate an increased Na+ conductance in respiratory epithelial cells from CF patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374371
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  • 19
    Electronic Resource
    Electronic Resource
    N-Acetyl-l-cysteine and its derivatives activate a Cl− conductance in epithelial cells (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 549-555 
    Details
    ISSN: 1432-2013
    Keywords: N-Acetyl-l-cysteine-S-Carboxymethyl-l-cysteine ; Respiratory epithelial cells ; Cystic fibrosis ; CFTR ; Cl− conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract N-Acetyl-l-cysteine (NAC) is a widely used mucolytic drug in patients with a variety of respiratory disorders including cystic fibrosis (CF). The beneficial effects of NAC are empirical and the exact mechanism of action in the airways remains obscure. In the present study we examined the effects on whole-cell (we) conductance (G m) and voltage (V m) of NAC and the congeners S-carboxymethyl-l-cysteine (CMC) andS-carbamyl-L-cysteine (CAC) andL-cysteine in normal and CF airway epithelial cells.L-Cysteine (1 mmol/1) had no detectable effect. The increase inG m (ΔGm) by the other compounds was concentration dependent and was (all substances at 1 mmol/1) 3.8 ± 1.4 nS (NAC; n = 11), 4.2 ± 1.0 nS (CMC;n = 16) and 3.8 ± 1.6 nS (CAC;n = 18), respectively. The changes in Gm were paralleled by an increased depolarization (ΔVm) when extracellular Cl− concentration was reduced to 34 mmol/1: under control conditions = -4.1 ± 2.1 versus 10.2 ± 2.1 mV in the presence of NAC, CMC, CAC (n = 36). In the presence of NAC, CMC and CAC, the reduction in Cl− concentration was paralleled by a reduction ofG m by 2.1 ± 0.4 nS (n = 35), indicating that all substances acted by increasing the Cl− conductance. Analysis of intracellular pH did not reveal any changes by any of the compounds (1 mmol/1). A Cl− conductance was also activated in HT29 colonic carcinoma and CF tracheal epithelial (CFDE) cells but not in CFPA1 cells, which do not express detectable levels of ΔF508-CFTR, suggesting that the presence of CFTR may be a prerequisite for the induction of Cl− currents. Next we examined the ion currents in Xenopus oocytes microinjected with CFTR-cRNA. Water-injected oocytes did not respond to activation by forskolin and 3-isobutyl-l-methylxanthine (IBMX) (ΔGm = 0.08 ±0.04 μS;n = 10) and no current was activated when these oocytes were exposed to NAC or CMC. In contrast, in CFTR-cRNA-injected cocytesG m was enhanced when intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) was increased by forskolin and IBMX (G m = 4.5 ± 1.3 μS;n = 8).G m was significantly increased by 0.74 ± 0.2 μS (n = 11) and 0.46 ± 0.1 μS (n = 10) when oocytes were exposed to NAC and CMC, respectively (both I mmol/1). In conclusion, NAC and its congeners activate Cl− conductances in normal and CF airway epithelial cells and hence induce electrolyte secretion which may be beneficial in CF patients. CFTR appears to be required for this response in an as yet unknown fashion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02191902
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  • 20
    Electronic Resource
    Electronic Resource
    Isolated perfused rabbit colon crypts: stimulation of Cl− secretion by forskolin (1993)
    Springer
    Pflügers Archiv 425 (1993), S. 373-380 
    Details
    ISSN: 1432-2013
    Keywords: Isolated perfused colon crypt ; Basolateral membrane voltage ; Cl− conductance ; Forskolin ; Loop diuretics ; Cl− secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to characterize ion conductances and carrier mechanisms of isolated in vitro perfused rabbit colonic crypts. Crypts were isolated from rabbit colon mucosa and mounted on a pipette system which allowed controlled perfusion of the lumen. In non-stimulated conditions basolateral membrane voltage (V b1) was −65±1 mV (n=240). Bath Ba2+ (1 mmol/ l) and verapamil (0.1 mmol/l) depolarized V b1 by 21±2 mV (n=7) and 31±1 (n=4), respectively. Lowering of bath Cl− concentration hyperpolarized V b1 from −69±3 to −75±3 mV (n=9). Lowering of luminal Cl− concentration did not change V b1. Basolateral application of loop diuretics (furosemide, piretanide, bumetanide) had no influence on V b1 in non-stimulated crypts. Forskolin (10−6 mol/l) in the bath depolarized V b1 by 29±2 mV (n=54) and decreased luminal membrane resistance. In one-third of the experiments a spontaneous partial repolarization of V b1 was seen in the presence of forskolin. During forskolin-induced depolarization basolateral application of loop diuretics hyperpolarized V b1 significantly and concentration dependently with a potency sequence of bumetanide 〉 piretanide ≥ furosemide. Lowering bath Cl− concentration hyperpolarized V b1. Lowering of luminal Cl− concentration from 120 to 32 mmol/l during forskolin-induced depolarization led to a further depolarization of Vb1 by 7±2 mV (n=10). We conclude that Vb1 of rabbit colonic crypt cells is dominated by a K+ conductance. Stimulation of the cells by forskolin opens a luminal Cl− conductance. Basolateral uptake of Cl− occurs via a basolateral Na+ : 2Cl− : K+ cotransport system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374861
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