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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: 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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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Does stimulation of NaCl secretion in in vitro perfused rectal gland tubules of Squalus acanthias increase membrane capacitance? (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 538-544 
    Details
    ISSN: 1432-2013
    Keywords: Key words CFTR ; Cl ; channels ; Cl ; secretion ; Endocytosis ; Exocrine secretion ; Exocytosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  NaCl secretion in rectal gland tubules (RGT) of Squalus acanthias requires the activation of Cl– channels in the luminal membrane. The RGT and its mechanism of activation are an early evolutionary paradigm of exocrine secretion. The respective Cl– channels probably resemble the shark equivalent of the cystic fibrosis transmembrane conductance regulator (CFTR). Activation of these Cl– channels occurs via cAMP. It has been hypothesized that the activation of CFTR occurs via exocytosis or inhibited endocytosis. To examine this question directly by electrical measurements we have performed whole-cell patch-clamp analyses of in vitro perfused RGT. NaCl secretion was stimulated by a solution (Stim) containing forskolin (10 µmol/l), dibutyryl-cAMP (0.5 mmol/l) and adenosine (0.5 mmol/l). This led to the expected strong depolarization and an increase in membrane conductance (G m). The membrane capacitance (C m) was measured by a newly devised two-frequency synchronous detector method. It was increased by Stim significantly from 5.00±0.22 to 5.17±0.21 pF (n=50). The increase in C m correlated with the increase in G m with a slope of 51 fF/nS. Next the effect of furosemide (500 µmol/l) was examined in previously stimulated RGT. Furosemide was supposed to inhibit coupled Na+2Cl–K+ uptake and to reduce cell volume but not membrane trafficking of Cl– channels. Furosemide reduced G m slightly (due to the fall in cytosolic Cl– concentration) and C m to the same extent by which Stim had increased it. Both changes were statistically significant, and the slope of ΔC m/ΔG m was similar to that caused by Stim. Inhibitors of microtubules or actin (colchicine, phalloidin and cytochalasin D added at 10 µmol/l to the pipette solution and dialysed for 〉10 min) did not alter cell voltage, G m or C m, nor did these inhibitors abolish the stimulatory effect of cAMP. These data suggest that the small C m changes observed with Stim reflect a minor cell volume increase and an ”unfolding” of the plasma membrane. The present data do not support the exocytosis/endocytosis hypothesis of cAMP-mediated activation of Cl– channels in these cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050669
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  • 4
    Electronic Resource
    Electronic Resource
    The basolateral Ca2+-dependent K+ channel in rat colonic crypt cells (1997)
    Springer
    Pflügers Archiv 435 (1997), S. 267-272 
    Details
    ISSN: 1432-2013
    Keywords: Key words K+ channel ; Colon crypt ; Ca2+ regulation ; Cl ; secretion ; ATP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Previous studies have indicated that a 16-pS K+ channel (KCca) in the basolateral membrane is responsible for the acetylcholine-induced whole-cell K+ conductance in these cells. In the present study we have examined this channel in excised inside-out patches of the basolateral membrane. Over a wide voltage range this channel showed inward rectification. The Ca2+ sensitivity was very marked, with a Hill coefficient of three and with half-maximal activation at 330 nmol/l. After several minutes most channels showed a slow run-down. Channel activity could be refreshed by addition of ATP (1 mmol/l) to the bath solution. The non-metabolizable derivative 5’-adenylylimidodiphosphate (AMP-PNP) had no such effect. In contrast, it inhibited channel activity by some 50%. ATP and its derivatives had no effect on the Ca2+ sensitivity. Channels activated by ATP were subsequently studied in the presence of alkaline (10 kU/l) or acidic (1 kU/l) phosphatase. Both phosphatases reduced channel activity significantly. These data suggest that the 16-pS K+ channel is directly controlled by cytosolic Ca2+. This regulatory step is probably distal to an activation produced by protein-kinase-C-dependent phosphorylation. As is the case for several other K+ channels, high concentrations of non-metabolizable ATP analogues inhibit this channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050511
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  • 5
    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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  • 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
    The cellular mechanisms of Cl– secretion induced by C-type natriuretic peptide (CNP). Experiments on isolated in vitro perfused rectal gland tubules of Squalus acanthias (1999)
    Springer
    Pflügers Archiv 438 (1999), S. 15-22 
    Details
    ISSN: 1432-2013
    Keywords: Key words cGMP ; Cl ; secretion ; C-type natriuretic peptide ; NaCl secretion ; Squalus acanthia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We have examined the mechanism whereby C-type natriuretic peptide (CNP), an agonist acting through the second messenger cGMP, enhances NaCl secretion in the rectal gland of Squalus acanthias. Single rectal gland tubules (RGT) were dissected manually, perfused in vitro and equivalent short-circuit current [I sc=transepithelial voltage/transepithelial resistance (R te)] as well as basolateral membrane voltage (V bl) were measured. CNP was added to luminal and basolateral perfusates at concentrations between 1 and 1000 nmol/l and its effects on the above parameters were compared to those of a ”stimulation cocktail” (Stim, containing dibutyryl cAMP, adenosine and forskolin) that maximally enhances cytosolic cAMP, and other agonists and hormones such as guanylin, vasoactive intestinal peptide (VIP), and adenosine. CNP had no effect from the luminal side (n=6). Its effects from the basolateral side consisted of a substantial increase in I sc (–31.6±7.7 to –316±82.2 µA/cm2, n=15). CNP significantly depolarized the luminal membrane from –87.4±1.0 to –82.3±2.6 mV (n=12). V bl was not changed (n=12) but the fractional conductance for K+ was increased (n=3). These effects were qualitatively and even quantitatively comparable to those of other agonists acting via cytosolic cAMP, but were less marked than those caused by Stim (n=64). The effects of VIP and CNP on I sc were not additive (n=5). The cytosolic Ca2+ concentration ([Ca2+]i) was monitored using the fura-2 fluorescence ratio (FFR 340/380 nm) and it was found that CNP, like agonists acting via cAMP, enhances FFR significantly from 1.02±0.05 to 1.32±0.05 (n=8) with a time constant in the 1–2 min in range. Our data suggest that CNP, acting via the second messenger cGMP, induces a marked increase in I sc in the rectal gland. The concomitant fall in R te corresponds to increases in the luminal membrane Cl– conductance and in the basolateral membrane K+ conductance. The latter effect is probably due to an increase in [Ca2+]i.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050874
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  • 8
    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: Key wordsN-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 (wc) conductance (G m) and voltage (V m) of NAC and the congeners S-carboxymethyl-L-cysteine (CMC) and S-carbamyl-L-cysteine (CAC) and L-cysteine in normal and CF airway epithelial cells. L-Cysteine (1 mmol/l) had no detectable effect. The increase in G m (ΔG m) by the other compounds was concentration dependent and was (all substances at 1 mmol/l) 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 G m were paralleled by an increased depolarization (ΔV m) when extracellular Cl− concentration was reduced to 34 mmol/l: 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 of G 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/l). A Cl− conductance was also activated in HT29 colonic carcinoma and CF tracheal epithelial (CFDE) cells but not in CFPAC-1 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-1-methylxanthine (IBMX) (ΔG m = 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 oocytes G 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 1 mmol/l). 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/s004240050034
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  • 9
    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: Key words 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% of G m was present in all cell types. A Na+ conductance was demonstrable in s.c. by the hyperpolarizing effect on V m of a low-Na+ (5 mmol/l) solution. In m.c. and b.c. the hyperpolarizing effect was much smaller, albeit significant. Amiloride had a concentration-dependent hyperpolarizing effect on V m in m.c. and even more so in s.c.. It reduced G 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) depolarized V 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 of V m and increase in G 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/l. This manoeuvre hyperpolarized V m under control conditions significantly by 6–9 mV in all three types of cells, whilst it depolarized V 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 triamterene-inhibitable Na+ conductance. m.c. and b.c. possess little or no Na+ conductance; their V 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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  • 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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