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  • Patch clamp  (15)
  • Exocrine secretion  (14)
  • Cl− conductance  (11)
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  • 1
    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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  • 2
    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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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Potassium conductance of smooth muscle cells from rabbit aorta in primary culture (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 57-68 
    Details
    ISSN: 1432-2013
    Keywords: Vascular smooth muscle cell ; K+ conductance ; Big Ca2+-dependent K+ channel ; Patch clamp ; Verapamil ; Protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vascular smooth muscle cells were obtained from rabbit aorta and were studied in primary culture on days 1–7 after seeding with electrophysiological techniques. In impalement experiments a mean membrane potential difference (PD) of −50±0.3 mV (n=387) was obtained with Ringer-type solution in the bath. PD was depolarized by 6±0.3 mV (n=45) and 16±2 mV (n= 5) when the bath K+ concentration was increased from the control value of 3.6 mmol/l to 13.6 and 23.6 mmol/l, respectively. Ba2+ (0.1–1 mmol/l) depolarized PD. Tetraethylammonium (TEA, 10 mmol/l) depolarized PD only slightly but significantly. Verapamil (0.1 mmol/l) and charybdotoxin (10 nmol/l) had no effect on PD. The conductance properties of these cells were further examined with the patch-clamp technique. K+ channels were spontaneously present in cell-attached patches. When the pipette was filled with 145 mmol/l KCl, a mean conductance (g K) of 209.6±4.6 mV (n=17) was read from the current/voltage curves at a clamp voltage (V c) of 0 mV. After excision K+ channels were found in 129 patches with inside-out and in 50 with outside-out configuration. With KCl on one and NaCl on the other side the mean g K at a V c of 0 mV was 134.6±3.9 pS (n=179). The mean permeability was 0.89±0.03×10−12 cm3/s. With symmetrical KCl solution the mean g K was 227±6 pS (n=17). The conductance sequence was g K≫ g Rb= g Cs=g Na=0. TEA blocked dose-dependently only from the outside.(1–10 mmol/l). Lidocaine (5 mmol/l) quinidine (0.01–1 mmol/l) and quinine (0.01–1 mmol/l) blocked from both sides. Charybdotoxin (0.5–5 nmol/l) blocked only from the extracellular side. Ba2+ blocked from the cytosolic side and the inhibition was increased by depolarization and reduced by hyperpolarization. At a V c of 0 mV a half-maximal inhibition (IC50) of 2 μmol/l was obtained. Verapamil and diltiazem blocked from both sides, verapamil with an IC50 of 2 μmol/l and diltiazem with an IC50 of 10 μmol/l. The open probability of this channel was increased by Ca2+ on the cytosolic side at activities 〉 0.1 μmol/l. Half-maximal activation occurred at Ca2+ activities exceeding 1 μmol/l. The present data indicate that the vascular smooth muscle cells of rabbit aorta in primary culture possess a K+ conductance. In excised patches only a maxi K+ channel was detected. This channel has properties different from the macroscopic K+ conductance. Hence, it is likely that the K+ conductance of the intact cell is dominated by yet another and thus far not detected K+ channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373748
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  • 6
    Electronic Resource
    Electronic Resource
    Cation specificity and pharmacological properties of the Ca2+-dependent K+ channel of rat cortical collecting ducts (1993)
    Springer
    Pflügers Archiv 422 (1993), S. 481-491 
    Details
    ISSN: 1432-2013
    Keywords: Patch clamp ; Verapamil ; Charyb-dotoxin ; Apamin ; K+ channel blocker ; Permselectivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The luminal membrane of principal cells of rat cortical collecting duct (CCD) is dominated by a K+ conductance. Two different K+ channels are described for this membrane. K+ secretion probably occurs via a small-conductance Ca2+-independent channel. The function of the second, large-conductance Ca2+-dependent channel is unclear. This study examines properties of this channel to allow a comparison of this K+ channel with the macroscopic K+ conductance of the CCD and with similar K+ channels from other preparations. The channel is poorly active on the cell. It has a conductance of 263±11 pS (n=36, symmetrical K+ concentrations) and of 139±3 pS (n=91) with 145 mmol/l K+ on one side and 3.6 mmol/l K+ on the other side of the membrane. Its open probability is high after excision (0.71±0.03, n=85). The channel flickers rapidly between open and closed states. Its permeability in the cell-free configuration was 7.0±0.2×10−13 cm3/s (n=85). It is inhibited by several typical blockers of K+ channels such as Ba2+, tetraethylammonium, quinine, and quinidine and high concentrations of Mg2+. The Ca2+ antagonists verapamil and diltiazem also inhibit this K+ channel. As is typical for the maxi K+ channel, it is inhibited by charybdotoxin but not by apamin. The selectivity of this large-conductance K+ channel demonstrates significant differences between the permeability sequence (P K 〉 P Rb 〉 P NH4 〉 P Cs=P Li=P Na=P choline=0) and the conductance sequence (g K 〉 g NH4 〉 g Rb 〉 g Li=g choline 〉 g Cs=g Na=0). The only other cations that are significantly conducted by this channel besides K+ (g K at V c =∞ is 279±8 pS, n=88) are NH 4 + (g NH4=127±22 pS, n=10) and Rb+ (g Rb=36±5 pS, n=6). The K+ currents through this channel are reduced by high concentrations of choline+, Cs+, Rb+, and NH 4 + . These properties and the dependence of this channel on Ca2+ and voltage classify it as a “maxi” K+ channel. A possible physiological function of this channel is discussed in the accompanying paper.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00375076
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  • 7
    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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  • 8
    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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  • 9
    Electronic Resource
    Electronic Resource
    The Na+2Cl–K+ cotransporter in the rectal gland of Squalus acanthias is activated by cell shrinkage (1999)
    Springer
    Pflügers Archiv 438 (1999), S. 165-176 
    Details
    ISSN: 1432-2013
    Keywords: Key words Cell volume ; Cl ; secretion ; Exocrine secretion ; Na+2Cl ; K+ cotransporter ; Phalloidin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Effects of cAMP on Cl– secretion, intracellular Cl– activity and cell volume were studied in isolated perfused rectal gland tubules (RGT) of Squalus acanthias with electrophysiological and fluorescence methods. Recording of equivalent short-circuit current (I sc) showed that cAMP stimulates Na+Cl– secretion in a biphasic manner. The first and rapid phase corresponds to Cl– exit via the respective protein-kinase-A- (PKA-) phosphorylated Cl– conductance. The inhibitory effect of the loop diuretic furosemide (0.5 mmol/l, n=12) indicates that second phase reflects the delayed (1–2 min) activation of the Na+2Cl–K+ cotransporter. During the first phase cytosolic Cl– activity, as monitored by 6-methoxy-N-(3-sulfopropyl) quinolinium (SPQ) fluorescence, fell to 78% (n=23) of the control value. Concomitantly, a transient fall in cell volume was recorded by calcein fluorescence to 92% (n=5) of the control value. Preincubation of the RGT with phalloidin (0.1 mmol/l, n=6) or cytochalasin D (0.1 mmol/l, n=4) almost completely prevented the development of the second phase of I sc activation. When cytosolic Cl– activity was increased by exposing the RGT to a high K+ concentration (25 mmol/l), in the presence of mannitol to prevent volume increases, stimulation was unaffected and biphasic. In contrast, when cell volume was clamped to an increased value (115%, n=8) by removing extracellular NaCl, the second phase was abolished completely (n=11). These data suggest that the primary and key process for triggering the Na+2Cl–K+ cotransport is transient cell shrinkage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050895
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  • 10
    Electronic Resource
    Electronic Resource
    Actin-dependent activation of ion conductances in bronchial epithelial cells (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 682-690 
    Details
    ISSN: 1432-2013
    Keywords: Cl− conductance ; K+ conductance ; Brefeldin A ; Cytochalasin D ; Epithelial cells ; Actin ; Microtubules
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Activation of Cl− and K+ channels is necessary to drive ion secretion in epithelia. There is substantial evidence from previous reports that vesicular transport and exocytosis are involved in the regulation of ion channels. In the present study we examined the role of cytoskeletal elements and components of intracellular vesicle transport on ion channel activation in bronchial epithelial cells. To this end, cells were incubated with a number of different compounds which interact with either microtubules or actin microfilaments, or which interfere with vesicle transport in the Golgi apparatus. The effectiveness of these agents was verified by fluorescence staining of cellular microtubules and actin. The function was examined in 36Cl− efflux studies as well as in whole-cell (WC) patch-clamp and cell-attached studies. The cells were studied under control conditions and after exposure to (in mmol/l) ATP (0.1), forskolin (0.01), histamine (0.01) and hypotonic bath solution (HBS, NaCl 72.5). In untreated control cells, ATP primarily activated a K+ conductance whilst histamine and forskolin induced mainly a Cl− conductance. HBS activated both K+ and Cl− conductances. Incubation of the cells with brefeldin A (up to 100 μmol/l) did not inhibit WC current activation and 36Cl− efflux. Nocodazole (up to 170 μmol/l) reduced the ATP-induced WC current, and mevastatin (up to 100 μmol/l) the cell-swelling-induced WC current. Neither had any effect on the WC current induced by forskolin and histamine. Also 36Cl− efflux induced by HBS, ATP, forskolin and histamine was unaltered by these compounds. Similarly, colchicine (10 μmol/l) and taxol (6 μmol/l) affected neither 36Cl− efflux nor WC current induced by ATP, forskolin, histamine or HBS. In contrast, depolymerisation of actin by cytochalasin D (10 μmol/l) significantly attenuated 36Cl− effluxes and WC current activation by the above-mentioned agonists. Incubation with a C2 clostridial toxin (5 nmol/l) showed similar effects on WC currents. Moreover, when cytochalasin D (10 μmol/l), C2 clostridial toxins (5 nmol/l), or phalloidin (10 μmol/l) were added to the pipette filling solution current activation was markedly reduced. However, in excised inside-out membrane patches, cytochalasin D (10 μmol/l), G-actin (10 μmol/l) and phalloidin (10 μmol/l) had no effect. These data suggest that actin participates in the activation of ion channels in 16HBE14o- epithelial cells and support the concept that exocytosis is a crucial step in the regulation of Cl− and K+ channels in these cells.
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    URL: http://dx.doi.org/10.1007/BF00373989
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