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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
    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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  • 4
    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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  • 5
    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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  • 6
    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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  • 7
    Electronic Resource
    Electronic Resource
    Effects of the carcinogen dimethylhydrazine (DMH) on the function of rat colonic crypts (1996)
    Springer
    Pflügers Archiv 433 (1996), S. 254-259 
    Details
    ISSN: 1432-2013
    Keywords: Key words Dimethylhydrazine ; Carcinogenesis ; Cl ; secretion ; Na+ channel ; Amiloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Rats injected with dimethylhydrazine for 5 weeks (DMH, 40 mg/kg body weight) invariably develop colonic cancer after a latency of some 10–14 weeks. Preliminary studies have suggested that Na+ absorption by surface colonic crypt cells is attenuated in the preneoplastic period (8–12 weeks after the first injection of DMH). The present study of glucocorticoid-treated (dexamethasone 6 mg/kg body weight, s.c. 3 days or triamcinolone 30 mg/kg body weight, s.c. 3 days) rats was undertaken to examine the ion transport properties of rat distal colon during this period in more detail. Ussing chamber studies of the distal colon and whole-cell patch-clamp measurements in surface cells, mid-crypt cells and crypt-base cells obtained from isolated crypts were performed. In Ussing chamber studies the equivalent short-circuit current inhibitable by amiloride (10 μmol/l) DMH-treated rats was about 40% of control. In addition, the hyperpolarizing effect of amiloride (10 μmol/l) on membrane voltage (V m) was strongly attenuated in surface and mid-crypt cells of DMH-treated rats. Carbachol (CCH, 100 μmol/l), which predictably hyperpolarized surface, mid-crypt cells and crypt-base cells of control rats, had no significant effect on V m in DMH-treated rats, but increased membrane conductance (G m) significantly. This indicates that CCH probably activates both Cl–and K+ channels in all three colonic crypt compartments in the DMH-treated rats. Forskolin (5 μmol/l), which has the most pronounced effect in crypt-base cells in control rats, depolarized V m and enhanced G m in all three compartments in DMH-treated rats. These data indicate that DMH profoundly alters Na+ and Cl–transport in colonic crypts prior to the appearance of colonic adenocarcinoma and that these effects can be summarized as follows: (1) the Na+ conductance of surface cells is attenuated; (2) cells along the length of the crypt-lumen axis tend to lose their normal response to CCH and instead show simultaneous and comparable increases in K+and Cl–conductances; (3) the effect of forskolin is enhanced along the entire crypt axis. As a result colonic crypt transport is shifted to predominant Cl–secretion, findings which are characteristic of colonic carcinoma cell lines such as HT29 and T84 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050275
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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: 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 dexamethasone were performed to examine the effects of stimulation by forskolin (10 μmol/1). 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/1 led to a hyperpolarization ofV 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/1. A reduction in bath Cl− concentration from 145 to 32 mmol/1 caused a depolarization ofV 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/1) Na+ concentrations:V m was hyperpolarized from −46 ± 4 to −62 ± 6 mV (n = 13). If the effect of Na+ onV 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+ onV m, the effects of increasing concentrations of several loop diuretics were examined. Furosemide, piretanide, torasemide and burnetanide (up to 0.1–0.5 mmol/1) all hyperpolarizedV 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 hyperpolarizedV m from −46 ± 3 to −74 ± 2 mV (n = 18) and reducedG 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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