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  • Exocrine secretion  (14)
  • Carbachol  (11)
  • 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
    8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8) acts as a muscarinic receptor antagonist in the epithelial cell line HT29 (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 295-301 
    Details
    ISSN: 1432-1912
    Keywords: Key words TMB-8 ; Fura-2 ; HT29 ; M3-receptor ; ATP ; Carbachol ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  8-(N, N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) is a widely used pharmacological tool to investigate the involvement of intracellular Ca2+ stores in cellular responses. In this study we investigate the effect of TMB-8 as a putative inhibitor of “Ca2+ signalling” in single fura-2 loaded HT29 colonic epithelial cells stimulated by ATP, carbachol (CCH) and neurotensin (NT). TMB-8 effectively inhibited the CCH-induced (100 μmol/l intracellular Ca2+ ([Ca2+]i) transient with an IC50 of 20 μmol/l. However, [Ca2+]i transients induced by other phospholipase C coupled agonists ATP (10 μmol/l, n=4) and NT (10 nmol/l, n=4) remained unaffected by TMB-8 (50 μmol/l). The agonist-induced [Ca2+]i transients remained equally unaffected by 100 μmol/l TMB-8 when the stimulatory concentration was reduced to 0.5 μmol/l for ATP (n=4) or 1 nmol/l for NT (n=4). The competitive nature of the TMB-8-induced inhibition of the CCH-induced [Ca2+]i transient was demonstrated by examining the agonist at various concentrations in absence and presence of the antagonist. High TMB-8 concentrations (100 μmol/l) alone induced a small [Ca2+]i increase (Δ[Ca2+]i: 40±5 nmol/l, n=7). We assume that this increase is a consequence of a TMB-8 induced intracellular alkalinization (ΔpH: 0.1±0.02, n=7) occurring simultaneously with the increase in [Ca2+]i. From these results we draw the following conclusions: (1) In sharp contrast to a large number of other studies, but in agreement with studies in other types of cells, these results substantially challenge the value of the “tool” TMB-8 as an “intracellular Ca2+ antagonist”; (2) TMB-8 acts a muscarinic receptor antagonist at the M3 receptor; (3) TMB-8 does not influence the release of Ca2+ from intracellular stores when IP3 signal transduction is activated by ATP or NT; (4) TMB-8 as a weak organic base alkalinizes the cytosol at high concentrations; and (5) TMB-8 induces small [Ca2+]i transients at higher concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168631
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  • 4
    Electronic Resource
    Electronic Resource
    8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8) acts as a muscarinic receptor antagonist in the epithelial cell line HT29 (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 295-301 
    Details
    ISSN: 1432-1912
    Keywords: TMB-8 ; Fura-2 ; HT29 ; M3-receptor ; ATP ; Carbachol ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 8-(N, N-diethyl amino) octyl-3,4,5-trimethoxybenzoate (TMB-8) is a widely used pharmacological tool to investigate the involvement of intracellular Ca2+ stores in cellular responses. In this study we investigate the effect of TMB-8 as a putative inhibitor of “Ca2+ signalling” in single fura-2 loaded HT29 coIonic epithelial cells stimulated by ATP, carbachol (CCH) and neurotensin (NT). TMB-8 effectively inhibited the CCH-induced (100 μmol/l intracellular Ca2+ ([Ca2+]i) transient with an IC50 of 20 μmol/l. However, [Ca2+]i transients induced by other phospholipase C coupled agonists ATP (10 μmol/l, n = 4) and NT (10 nmol/l, n = 4) remained unaffected by TMB-8 (50 μmol/l). The agonist-induced [Ca2+]i transients remained equally unaffected by 100 μmol/l TMB-8 when the stimulatory concentration was reduced to 0.5 μmol/I for ATP (n = 4) or 1 nmol/l for NT (n = 4). The competitive nature of the TMB-8-induced inhibition of the CCH-induced [Ca2+]i transient was demonstrated by examining the agonist at various concentrations in absence and presence of the antagonist. High TMB-8 concentrations (100 μmol/l) alone induced a small [Ca2+]i increase (Δ[Ca2+]i: 40 ± 5 nmol/l, n = 7). We assume that this increase is a consequence of a TMB-8 induced intracellular alkalinization (Δ pH: 0.1 ± 0.02, n = 7) occurring simultaneously with the increase in [Ca +]i. From these results we draw the following conclusions: (1) In sharp contrast to a large number of other studies, but in agreement with studies in other types of cells, these results substantially challenge the value of the “tool” TMB-8 as an “intracellular Ca2+ antagonist”; (2) TMB-8 acts a muscarinic receptor antagonist at the M3 receptor; (3) TMB-8 does not influence the release of Ca2+ from intracellular stores when IP3 signal transduction is activated by ATP or NT; (4) TMB-8 as a weak organic base alkalinizes the cytosol at high concentrations; and (5) TMB-8 induces small [Ca2+]i transients at higher concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168631
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  • 5
    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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  • 6
    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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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Attenuation of stimulated Ca2+ influx in colonic epithelial (HT29) cells by cAMP (1996)
    Springer
    Pflügers Archiv 432 (1996), S. 735-740 
    Details
    ISSN: 1432-2013
    Keywords: Key words Ca2+ influx ; Fura-2 ; cAMP ; Forskolin ; Carbachol ; HT29 ; Second messenger ; Patch-clamp technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In HT29 colonic epithelial cells agonists such as carbachol (CCH) or ATP increase cytosolic Ca2+ activity ([Ca2+]i) in a biphasic manner. The first phase is caused by inositol 1,4,5-trisphophate-(Ins P 3-) mediated Ca2+ release from their respective stores and the second plateau phase is mainly due to stimulated transmembraneous Ca2+ influx. The present study was undertaken to examine the effect of increased adenosine 3′,5′-cyclic monophasphate (cAMP) (forskolin 10 μmol/l = FOR) on the Ca2+ transient in the presence of CCH (100 μmol/l). In unpaired experiments it was found that FOR induced a depolarization and reduced cytosolic Ca2+ ([Ca2+]i, measured as the fura-2 fluorescence ratio 340/380 nm) significantly. Dideoxyforskolin had no such effect. The effect of FOR was abolished when the cells were depolarized by a high-K+ solution. In further paired experiments utilizing video imaging in conjunction with whole-cell patch-clamp, [Ca2+]i was monitored separately for the patch-clamped cell and three to seven neighbouring cells. In the presence of CCH, FOR reduced [Ca2+]i uniformly from a fluorescence ratio (345/380) of 2.9 ± 0.12 to 1.8 ± 0.07 in the patch-clamped cell and its neighbours (n = 48) and depolarized the membrane voltage (V m) of the patch-clamped cells significantly and reversibly from −54 ± 7.4 to −27 ± 5.9 mV (n = 6). In additional experiments V m was depolarized by 15–54 mV by various increments in the bath K+ concentration. This led to corresponding reductions in [Ca2+]i. Irrespective of the cause of depolarization (high K+ or FOR) there was a significant correlation between the change in V m and change in [Ca2+]i. These data indicate that the cAMP-mediated attenuation of Ca2+ influx is caused by the depolarization produced by this second messenger.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050192
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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Effect of intracellular pH on agonist-induced [Ca2+]i transients in HT29 cells (1997)
    Springer
    Pflügers Archiv 434 (1997), S. 466-474 
    Details
    ISSN: 1432-2013
    Keywords: Key words BCECF ; Fura-2 ; pHi ; [Ca2+]i ; HT29 ; Carbachol ; Neurotensin ; ATP ; InsP3 ; Cell volume ; Calcein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In this study we examined the influence of intracellular pH (pHi) on agonist-induced changes of intracellular Ca2+ activity ([Ca2+]i) in HT29 cells. pHi and [Ca2+]i were measured microspectrofluorimetrically using BCECF and fura-2, respectively. Buffers containing trimethylamine (TriMA), NH3/NH4 + and acetate were used to clamp pHi to defined values. The magnitudes of the peak and plateau of [Ca2+]i transients induced by carbachol (CCH, 10–6 mol/l) were greatly enhanced by an acidic pHi and nearly abolished by an alkaline pHi. The relationship between pHi and the [Ca2+]i peak was nearly linear from pHi 7.0 to 7.8. This effect of pHi was also observed at higher CCH concentrations (10–4 and 10–5 mol/l), at which the inhibitory effect of an alkaline pHi was more pronounced than the stimulatory effect of an acidic pHi. An acidic pHi shifted the CCH concentration/response curve to the left, whereas an alkaline pHi led to a rightward shift. The influence of pHi on [Ca2+]i transients induced by neurotensin (10–8 mol/l) or ATP (5 × 10–7 mol/l) was similar to its influence on those induced by CCH, but generally not as pronounced. Measurements of cellular inositol 1,4,5-trisphosphate (InsP 3) showed no changes in response to acidification with acetate (20 mmol/l) or alkalinization with TriMA (20 mmol/l). The InsP 3 increase induced by CCH was unaltered at an acidic pHi, but was augmented at an alkaline pHi. Confocal measurements of cell volume showed no significant changes induced by TriMA or acetate. Slow-whole-cell patch-clamp experiments showed no additional effect of CCH on the membrane voltage (V m) measured after TriMA or acetate application. We conclude that pHi is a physiological modulator of hormonal effects in HT29 cells, as the [Ca2+]i responses to agonists were significantly changed at already slightly altered pHi. The measurements of InsP 3, cell volume and V m show that pHi must act distally to the InsP 3 production, and not via changes of cell volume or V m.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050422
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