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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
    Proceedings of the Australian Physiological and Pharmacological Society Symposium: Ion Channels EXPRESSION AND FUNCTION OF COLONIC EPITHELIAL KVLQT1 K+ CHANNELS (2001)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 28 (2001), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. KVLQT1 (KCNQ1) is a voltage-gated K+ channel essential for repolarization of the heart action potential. Defects in ion channels have been demonstrated in cardiac arrhythmia. This channel is inhibited potently by the chromanol 293B. The same compound has been shown to block cAMP-dependent electrolyte secretion in rat and human colon. Therefore, it was suggested that a K+ channel similar to KVLQT1 is expressed in the colonic epithelium.2. In the present paper, expression of KVLQT1 and its function in colonic epithelial cells is described. Reverse transcription–polymerase chain reaction analysis of rat colonic mucosa demonstrated expression of KVLQT1 in both crypt cells and surface epithelium. When expressed in Xenopus oocytes, KVLQT1 induced a typical delayed activated K+ current.3. As demonstrated, the channel activity could be further activated by increases in intracellular cAMP. These and other data support the concept that KVLQT1 is forming a component of the basolateral cAMP-activated K+ conductance in the colonic epithelium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2001.03407.x
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  • 4
    Electronic Resource
    Electronic Resource
    Glycoprotein nature of energy-transducing ATPases - Chemical characterization of glycopeptides isolated from bacterial and chloroplast coupling factors
    Amsterdam : Elsevier
    FEBS Letters 86 (1978), S. 1-5 
    Details
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(78)80084-2
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  • 5
    Electronic Resource
    Electronic Resource
    Eine Trennkammer fur die Hochspannungselektrophorese nach dem Michl'- schen Prinzip
    Amsterdam : Elsevier
    Journal of Chromatography A 33 (1968), S. 558-560 
    Details
    ISSN: 0021-9673
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0021-9673(00)98693-X
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  • 6
    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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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Evidence for Na+/Ca2+ exchange in the rectal gland of Squalus acanthias (1999)
    Springer
    Pflügers Archiv 439 (1999), S. 49-51 
    Details
    ISSN: 1432-2013
    Keywords: Cl– secretion cAMP Cytosolic Ca2+ Exocrine secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Previously we have shown that stimulation of in vitro perfused rectal gland tubules (RGT) of the dogfish Squalus acanthias by adenosine 3',5'-cyclic monophosphate (cAMP), (as a cocktail comprising 0.1 mmol/l dibutyryl-cAMP, 10 µmol/l forskolin and 0.1 mmol/l adenosine, hereafter termed STIM) leads to an increase in cytosolic Ca2+ ([Ca2+]i) and that this assists Cl– secretion by enhancing basolateral K+ conductance. In the present study we examined the mechanism of the cAMP-induced increase in [Ca2+]i. [Ca2+]i was measured using the fura-2 technique in isolated in vitro perfused RGT. As before, STIM enhanced [Ca2+]i. This elevation of [Ca2+]i was prevented completely when STIM was added in the presence of the Na+2Cl–K+ cotransport inhibitor furosemide (0.5 mmol/l). This suggests that the increase in [Ca2+]i induced by STIM is caused by a concomitant increase in cytosolic Na+ ([Na+]i) and not by the activation of second messenger cascades. Furosemide prevents this increase in [Na+]i and hence the elevation of [Ca2+]i. Moreover, the plateau phase of the [Ca2+]i transient produced by carbachol (CCH, 0.1 mmol/l) was augmented strongly when bath Na+ was reduced to 5 mmol/l. These data suggest that the level of [Ca2+]i is determined by Na+-dependent Ca2+ export, most likely via a Na+/Ca2+ exchanger. The increase in [Na+]i accompanying stimulation of Cl– secretion reduces the rate of Ca2+ export leading to an elevation of [Ca2+]i, as does a reduction in bath Na+ which augments the [Ca2+]i plateau produced by CCH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004249900163
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  • 9
    Electronic Resource
    Electronic Resource
    Regulation of the Na+2Cl–K+ cotransporter in isolated rat colon crypts (2000)
    Springer
    Pflügers Archiv 439 (2000), S. 378-384 
    Details
    ISSN: 1432-2013
    Keywords: cAMP Carbachol Cl– secretion Exocrine secretion K+ channels Volume regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The Na+2Cl–K+ cotransporter accepts NH4 + at its K+-binding site. Therefore, the rate of cytosolic acidification after NH4 + addition to the bath (20 mmol/l) measured by BCECF fluorescence can be used to quantify the rate of this cotransporter. In isolated colon crypts of rat distal colon (RCC) addition of NH4 + 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 (Δ fluorescence ratio units/1000 s). In pilot experiments it was shown that the pH signal caused by the Na+2Cl–K+ cotransporter could be amplified if the experiments were carried out in the presence of bath Ba2+ to inhibit NH4 + uptake via K+ channels. Therefore all subsequent experiments were performed in the presence of 1 mmol/l Ba2+. In the absence of any secretagogue, preincubation of RCC in a low-Cl– solution (4 mmol/l) for 10 min enhanced the uptake rate significantly from 1.70±0.11 to 2.54±0.27 U/1000 s (n=20). The addition of 100 mmol/l mannitol (hypertonic solution) enhanced the rate significantly from 1.93±0.17 to 2.84±0.43 U/1000 s (n=5). Stimulation of NaCl secretion by a solution containing 100 µmol/l carbachol (CCH) led to a small but significant increase in NH4 + uptake rate from 2.06±0.34 to 2.40±0.30 U/1000 s (n=11). The increase in uptake rate observed with stimulation of the cAMP pathway by isobutylmethylxanthine (IBMX) and forskolin (100 µmol/l and 5 µmol/l, respectively) was from 2.39±0.24 to 3.06±0.36 U/1000 s (n=24). Whatever the mechanism used to increase the NH4 + uptake rate, azosemide (500 µmol/l) always reduced this rate to control values. Hence three manoeuvres enhanced loop-diuretic-inhibitable uptake rates of the Na+2Cl–K+ cotransporter: (1) lowering of cytosolic Cl– concentration; (2) cell shrinkage; (3) activation of NaCl secretion by carbachol and (4) activation of NaCl secretion by cAMP. The common denominator of all four activation pathways may be a transient fall in cell volume.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004249900156
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  • 10
    Electronic Resource
    Electronic Resource
    Deoxycholic acid (DOC) affects the transport properties of distal colon (2000)
    Springer
    Pflügers Archiv 439 (2000), S. 532-540 
    Details
    ISSN: 1432-2013
    Keywords: Bile acid Cl– channels Deoxycholate Diarrhea K+ channels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Secondary bile acids can induce diarrhea. In the present study we examined the effects of deoxycholic acid (DOC) on equivalent short-circuit current (I sc) in rabbit colon and the cellular mechanisms involved in DOC action (rabbit and rat). Luminal DOC inhibited amiloride-sensitive Na+ absorption. In the presence of amiloride luminal DOC had a concentration dependent effect on I sc. Low concentrations (1–10 µmol/l) induced a lumen-positive current (51±3 µA/cm2, 10 µmol/l, n=7) which was inhibited by luminal Ba2+ suggesting the activation of a luminal K+ conductance. Higher luminal concentrations induced a lumen-negative current (–76±9 µA/cm2, 100 µmol/l, n=11). Basolateral application of DOC, also in the presence of amiloride, only induced lumen-negative I sc (–58±10 µA/cm2, 100 µmol/l, n=6, EC50=3 µmol/l). This current could be abolished completely by the K+ channel blocker 293B, a selective inhibitor of cAMP-dependent Cl– secretion. This action of DOC on I sc was additive to the effect of carbachol (CCH) but not additive to that of cAMP. In intact rat colon mucosa pretreated with DOC a significant increase in cAMP production was observed. Fura-2 measurements of cytosolic Ca2+ activity ([Ca2+]i) in isolated colonic crypts (rabbit and rat) showed that 100 µmol/l DOC induced a weak [Ca2+]i increase. Whole-cell measurements of membrane voltage in isolated rat colonic crypts revealed a hyperpolarization by DOC (–4.9±0.8 mV, 100 µmol/l, n=8) but a depolarization by prostaglandin E2 (PGE2, via cAMP) (24±7 mV, n=8). The present data show that DOC acts at more than one target in the colon: in the intact mucosa it activates luminal K+ channels and Cl– secretion and this is paralleled by an increase in cAMP production. In isolated crypts DOC probably activates a Ca2+-regulated K+ conductance but has no effect on cAMP. Hence DOC probably activates ion channels or channel-regulating factors in colonocytes and acts on non-epithelial cells to activate Cl– secretion indirectly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004249900226
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