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  • Electronic Resource  (20)
  • Patch clamp  (15)
  • Rat  (7)
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  • Electronic Resource  (20)
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  • 1
    Electronic Resource
    Electronic Resource
    Handling of allantoin by the rat kidney (1975)
    Springer
    Pflügers Archiv 357 (1975), S. 201-207 
    Details
    ISSN: 1432-2013
    Keywords: Allantoin ; Uricase ; Kidney ; Clearance ; Micropuncture ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Renal excretion of allantoin was measured by tracer techniques. After injection of 2-C14 urate and H3 inulin, clearances of allantoin and inulin were measured and both proximal and distal tubules were micropunctured. In confirmation of earlier results 2-C14 urate injected into an intact animal is very rapidly converted to C14 allantoin: after 15 min more than 90% of urinary tracer is present as allantoin. It was further observed that 1) allantoin clearance is essentially identical with inulin clearance over a wide range of urine flows; 2) no net transport of allantoin occurs in either proximal or distal tubules. Clearly allantoin is handled by the rat kidney like inulin. The total excretion of filtered allantoin unlike that of filtered urate provides an easy and effective mechanism for animals possessing the enzyme uricase to dispose of their purine loads.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585975
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  • 2
    Electronic Resource
    Electronic Resource
    Diphenylamine-2-carboxylate, a blocker of the Cl−-conductive pathway in Cl−-transporting epithelia (1985)
    Springer
    Pflügers Archiv 405 (1985), S. S95 
    Details
    ISSN: 1432-2013
    Keywords: Cl−-Channel ; Rectal gland ; Thick ascending limb of the loop of Henle ; Cl−-Secretion ; Cl−-Reabsorption ; Patch clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study examines the effects of diphenylamine-2-carboxylate (DPC) in Cl−-transporting epithelia. This substance blocks reversibly the Cl−-conductance present under normal circumstances in the basolateral membrane of the thick ascending limb of the loop of Henle (TAL) and in the apical membrane of shark rectal gland tubules (RGT). This leads to a reduction in active NaCl reabsorption (TAL) and NaCl secretion (RGT) respectively, as measured by the equivalent short circuit current. The cells hyperpolarize as the membrane voltage drifts from the control value (some compromise between the chemical potential of Cl− and K+) towards the chemical potential of K+. The resistance of the basolateral (TAL) or apical membrane (RGT) increases and this leads to a moderate increase in transepithelial resistance. In addition, the Cl−-concentration step induced membrane voltage changes, which can be produced under control conditions, disappear in the presence of the blocker. Finally, experiments in excised membrane patches indicate that this substance inhibits the single current events of individual Cl−-channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581787
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  • 3
    Electronic Resource
    Electronic Resource
    Culture-dependent expression of Na+ conductances in airway epithelial cells (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 578-586 
    Details
    ISSN: 1432-2013
    Keywords: αhENaC ; Airway epithelial cells Amiloride ; CFTR ; Patch clamp ; RT-PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract According t0 previous studies, amiloride-sensitive (Amil+) Na+ channels are present in apical membranes of airway epithelial cells. When isolated from intact tissue and grown in primary culture 0r as immortalized cell lines, these cells tend t0 lose these Amil+ Na+ channels. The present study examines this issue in immortalized human bronchial epithelial cells (16HBE140- cell line). The mRNA of one subunit of the Na+ channel (αhENaC) was semi-quantified by polymerase chain reaction of reverse transcribed RNA. Transcripts were significantly increased when cells were exposed t0 aldosterone and dexamethasone irrespective of whether grown on permeable supports 0r plastic. When grown on plastic dishes 16HBE140-cells showed cAMP-dependent Cl− currents in whole-cell (WC) patch-clamp experiments, corresponding t0 expression of the cystic fibrosis transmembrane conductance regulator (CFTR). Na+ currents could not be detected although cells expressed significant amounts ofαhENaC as demonstrated by Northern blot analysis. In contrast, when cells were grown on permeable supports 0r cultured in the presence of butyrate (5 mmol/l, plastic 0r permeable support) 0r aldosterone and dexamethasone (both 1 μol/l, plastic 0r permeable support), amiloride (10 μmol/1) hyperpolarized the membrane voltage (ΔVm) by 2–9 mV paralleled by small reductions of WC conductances (ΔGm) of 0.4-4.0 nS. The effects of amiloride on ΔVm were generally more pronounced (up t0 12 mV) when cells were grown on permeable supports. The amiloride effect (ΔVm) was concentration dependent with an inhibitory constant, Ki, of about 0.1 μmol/l. We further examined whether the induction of an Amil+ Na+ conductance was paralleled by additional changes in membrane conductance. In fact, the cAMP-activated Cl− conductance was significantly attenuated by approximately 80% (n = 35) in cells responding t0 amiloride, whilst the ATP-activated K+ conductance remained unaffected. The present data suggest that cellular mechanisms determining differentiation control the functional expression of Na+ and Cl− conductances in human airway epithelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02191906
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  • 4
    Electronic Resource
    Electronic Resource
    cAMP-dependent activation of small-conductance Cl− channels in HT29 colon carcinoma cells (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 230-237 
    Details
    ISSN: 1432-2013
    Keywords: Cl− channels ; HT29 ; Isoproterenol ; α2 receptor ; cAMP ; Cell-attached nystatin ; Patch clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to examine the conductance properties in the colon carcinoma cell line HT29 and the activation of Cl− channels by cAMP. A modified cell-attached nystatin patch-clamp technique was used, allowing for the simultaneous recording of the cell membrane potential (PD) and the conductance properties of the cell-attached membrane. In resting cells, PD was −56±0.4 mV (n=294). Changing the respective ion concentrations in the bath indicate that these cells possess a dominating K+ conductance and a smaller Cl− conductance. A significant non-selective cation conductance, which could not be inhibited by amiloride, was only observed in cells examined early after plating. The K+ conductance was reversibly inhibited by 1–5 mmol/l Ba2+. Stimulation of the cells by the secretagogues isoproterenol and vasointestinal polypeptide (VIP) depolarized PD and induced a Cl− conductance. Similar results were obtained with compounds increasing cytosolic cAMP: forskolin, 3-isobutyl-1-methylxanthine, cholera toxin and 8-bromoadenosine cyclic 3′,5′-monophosphate (8-Br-cAMP). VIP (1 nmol/l, n=10) and isoproterenol (1 umol/l, n=12) depolarized the cells dose-dependently and reversibly by 12±2 mV and 13±2 mV. The maximal depolarization was reached after some 20 s. The depolarization was due to increases in the fractional Cl− conductance. Simultaneously the conductance of the cellattached membrane increased from 155±31 pS to 253±40 pS (VIP, n=4) and from 170±43 pS to 268±56 pS (isoproterenol, n=11), reflecting the gating of Cl− channels in the cell-attached membrane. 5-Nitro-2-(3-phenylpropylamino)-benzoate (1 μmol/l) was without significant effects in resting and in forskolin-stimulated HT29 cells. The agonist-induced conductance increase of the cell-attached nystatin patches was not paralleled by the appearance of detectable single-channel events in these membranes. These data suggest activation of small, non-resolvable Cl− channels by cAMP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374832
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  • 5
    Electronic Resource
    Electronic Resource
    Small-conductance Cl− channels in HT29 cells: activation by Ca2+, hypotonic cell swelling and 8-Br-cGMP (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 238-246 
    Details
    ISSN: 1432-2013
    Keywords: Cl− channels ; HT29 cells ; Ca2+-mobilizing hormones ; ATP ; Carbachol ; Neurotensin ; NPPB ; Patch clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study demonstrates the activation of Cl− channels in HT29 cells by agonist (ATP, neurotensin, carbachol) increasing cytosolic Ca2+, by hypotonic cell swelling and by cGMP. Cell-attached nystatin patch-clamp (CAN) as well as slow and fast wholecell recordings were used. The cell membrane potential was depolarized in a dose-dependent manner with halfmaximal effects at 0.4 umol/l for ATP, 60 pmol/l for neurotensin and 0.8 μmol/l for carbachol. The depolarization, which was caused by Cl− conductances increases, occurred within 1 s and was accompanied by a simultaneous and reversible increase of the input conductance of the cell-attached membrane from 295±32 pS to 1180±271 pS (ATP; 10 μmol/l, n=21) and 192±37 pS to 443±128 pS (neurotensin; 1 nmol/l, n=8). The effects of the agonists could be mimicked by ionomycin (0.2 umol/l), suggesting that an increase in intracellular Ca2+ was responsible for the activation of Cl− channels. The depolarization was followed by a secondary hyperpolarization. Hypotonic cell swelling also depolarized the cells and induced an increase in the membrane conductance. With 120 mmol/l NaCl the depolarization was 10±0.8 mV and the cell-attached conductance increased from 228±29 pS to 410±65 (n=26) pS. NaCl at 90 mmol/l and 72.5 mmol/l had even stronger effects. Comparable conductance increases were also obtained when the different agonists or hypotonic cell swelling were examined in whole cell experiments. 5-Nitro-2-(3-phenylpropylamino)-benzoate (1 μmol/l) did not prevent the effects of Ca2+-increasing hormones and of hypotonic solutions. An increase in Cl− conductance was also induced by 8-Br-cGMP (1 mmol/l) but not by heat-stable Escherichia coli toxin. In contrast to their conductance-increasing effects in CAN patches, the different agonists and cell swelling did not activate resolvable single channels in these cell-attached membranes. This indicates that the Cl− channels involved have a single-channel conductance too small (≤ 4 pS, 150 Hz) to be resolved by our techniques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374833
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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
    In vivo studies on uricase activity in the rat (1974)
    Springer
    Pflügers Archiv 351 (1974), S. 323-330 
    Details
    ISSN: 1432-2013
    Keywords: Uricase ; Urate ; Allantoin ; Liver ; Kidney ; Microperfusion ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. In vivo uricase activity was tested in rats by injection of 2-C14 urate and measurement of the total C14 activity and the fractional activities of allantoin, allantoic acid and urea in samples of blood and urine. In control animals, 5 min after the injection, 70% of the plasma tracer was already present in the form of allantoin. No allantoic acid and urea were produced. Intestinectomy had no measurable influence on uricase activity. On the other hand, hepatectomy or ligation of the hepatic artery combined with subtotal viscerectomy did abolish uricase activity almost completely. 2. Following microinjections into proximal tubules of Ringer solution containing 2-C14 urate, urine samples during early recovery mainly contained labelled urate, whereas in later samples the fraction of labelled allantoin increased. About 12 min after the microinjection the urine of both kidneys contained equal amounts of tracer mainly in the form of allantoin. 3. When segments of proximal tubules were perfused with an equilibrium solution containing tracer amounts of C 14 urate, no urate was metabolized during its passage through the proximal tubule. 4. C 14 urate was offered from the peritubular capillaries and samples of tubular fluid were analyzed, Again, all the tracer in the tubular fluid was in the form of urate, indicating that urate is not oxidized when it is transported across the tubular cell. It is concluded from these results that: 1. The rat kidney has no significant uricase activity. 2. Urate transport in the kidney is not influenced by this enzyme. 3. The degradation of urate to allantoin takes place at extrarenal sites, mainly in the liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00593318
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  • 8
    Electronic Resource
    Electronic Resource
    Na+ and Cl− conductances in airway epithelial cells: increased Na+ conductance in cystic fibrosis (1995)
    Springer
    Pflügers Archiv 431 (1995), S. 1-9 
    Details
    ISSN: 1432-2013
    Keywords: Na+ channel ; Respiratory epithelial cells ; Human Na+ channel ; Micropuncture ; Patch clamp ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Na+ and Cl− conductances in the apical membrane of respiratory epithelial cells are essential for electrolyte and water transport in the airways. Apart from the well described defect in adenosine 3′∶5′ cyclic monophosphate-(cAMP-) dependent activation of Cl− conductances in cystic fibrosis (CF), an increased Na+ conductance has also been reported from transepithelial measurements. In the present experiments we tried to identify these conductances in nasal epithelial cells using patch-clamp and microelectrode techniques. With these methods we found identical and relatively low membrane voltages of about −36 mV in both freshly isolated and primary cultured normal and CF nasal epithelial cells. A Cl− conductance could be activated by cAMP in normal (ΔG=3.1±0.8 nS, n=10) but not in CF (ΔG=0.3±0.1 nS, n=11) cells, whereas Ca2+-dependent Cl− currents activated by adenosine 5′-triphosphate (ATP) and bradykinin were present in both types of cells. Cell-attached membrane patches from stimulated cells did not reveal discernible singlechannel events when activated with any of the agonists. A Na+ conductance was also detected in freshly isolated ciliated respiratory cells in impalement studies, as evidenced by the hyperpolarization induced by 10 μmol/l amiloride (ΔV= −5.2±0.6 mV, n=56) and when Na+ was replaced in the bath by N-methyld-glucamine (NMDG) (ΔV = −5.7±0.9 mV, n=14). In whole-cell patch-clamp experiments, the amilorideinduced hyperpolarization was significantly larger in CF (ΔV = −9.7±2.4 mV, n=22) when compared to normal (ΔV = −3.3±0.9 mV, n=27) cells in short-term culture. Reverse transcriptase polymerase chain reaction analysis of normal respiratory cells identified messenger RNA of both the cystic fibrosis transmembrane conductance regulator (CFTR) as well as the human epithelial Na+ channel (hNaCh). The present experiments confirm the absence of a cAMP-dependent Cl− conductance in CF respiratory epithelial cells and support previous findings obtained in transepithelial and microelectrode studies which indicate an increased Na+ conductance in respiratory epithelial cells from CF patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374371
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  • 9
    Electronic Resource
    Electronic Resource
    Culture-dependent expression of Na+ conductances in airway epithelial cells (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 578-586 
    Details
    ISSN: 1432-2013
    Keywords: Key wordsαhENaC ; Airway epithelial cells ; Amiloride ; CFTR ; Patch clamp ; RT-PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract According to previous studies, amiloride-sensitive (Amil+) Na+ channels are present in apical membranes of airway epithelial cells. When isolated from intact tissue and grown in primary culture or as immortalized cell lines, these cells tend to lose these Amil+ Na+ channels. The present study examines this issue in immortalized human bronchial epithelial cells (16HBE14o-cell line). The mRNA of one subunit of the Na+ channel (αhENaC) was semi-quantified by polymerase chain reaction of reverse transcribed RNA. Transcripts were significantly increased when cells were exposed to aldosterone and dexamethasone irrespective of whether grown on permeable supports or plastic. When grown on plastic dishes 16HBE14o-cells showed cAMP-dependent Cl− currents in whole-cell (WC) patch-clamp experiments, corresponding to expression of the cystic fibrosis transmembrane conductance regulator (CFTR). Na+ currents could not be detected although cells expressed significant amounts of αhENaC as demonstrated by Northern blot analysis. In contrast, when cells were grown on permeable supports or cultured in the presence of butyrate (5 mmol/l, plastic or permeable support) or aldo-sterone and dexamethasone (both 1 μmol/l, plastic or permeable support), amiloride (10 μmol/l) hyperpolarized the membrane voltage (ΔV m) by 2–9 mV, paralleled by small reductions of WC conductances (ΔG m) of 0.4–4.0 nS. The effects of amiloride on ΔVm were generally more pronounced (up to 12 mV) when cells were grown on permeable supports. The amiloride effect (ΔV m) was concentration dependent with an inhibitory constant, K i, of about 0.1 μmol/l. We further examined whether the induction of an Amil+ Na+ conductance was paralleled by additional changes in membrane conductance. In fact, the cAMP-activated Cl− conductance was significantly attenuated by approximately 80% (n = 35) in cells responding to amiloride, whilst the ATP-activated K+ conductance remained unaffected. The present data suggest that cellular mechanisms determining differentiation control the functional expression of Na+ and Cl− conductances in human airway epithelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050038
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  • 10
    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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