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  • Cl− conductance  (11)
  • CFTR  (9)
  • Rat  (7)
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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
    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
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373989
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  • 4
    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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  • 5
    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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  • 6
    Electronic Resource
    Electronic Resource
    Swelling of rat mesangial cells induces a Ca2+-dependent Cl− conductance (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 706-712 
    Details
    ISSN: 1432-2013
    Keywords: Mesangial cell ; Cell swelling ; Ion currents ; Intracellular Ca2+ activity ; Cl− conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Membrane voltage (V m) and ion currents of rat mesangial cells in primary culture were measured with the patch-clamp technique in the fast whole-cell configuration.V m was −44 ± 1 mV (n = 138). A reduction of the osmolality from 290 to 190 mosmol/kg depolarizedV m from −44 ± 1 to −29 ± 1 mV (n = 118) and increased the inward and outward conductances (Gm) from 14±2 to 39 ± 4 nS and 13±2 to 37 ± 4 nS (n = 84), respectively. During the hypotonicity-induced depolarization the cell capacitance increased significantly from 33 ± 3 to 42 ± 4 pF (n = 40). The effect of hypotonic cell swelling onV m was increased in a bath with a reduced extracellular Cl− of 32 mmol/l (by 71 ± 4%,n = 23), indicating that a Cl− conductance was activated. The permselectivity of this conductance was I− ≥ Br− 〉 Cl−. TheV m response was not affected in the presence of a reduced extracellular Na+ of 5 mmol/l (n = 13) and was inhibited in a solution with reduced extracellular Ca2+ concentration (by 63 ± 9%,n = 14). In microfluorescence measurements with the Ca2+-sensitive dye fura-2 hypotonic cell swelling induced a sustained increase of the intracellular Ca2+ activity, [Ca2+]i (n = 19). The increase of [Ca2+]i was completely inhibited when the extracellular solution was free of Ca2+. TheV m response to hypotonic cell swelling was not attenuated in the presence of the L-type Ca2+ channel blockers nicardipine (n = 5), nifedipine (n = 5) and verapamil (n = 5) (all at 1 μmol/l). The data indicate that in rat mesangial cells, osmotic swelling induces a Ca2+ influx from extracellular space. This Ca2+ influx activates a Cl− conductance resulting in a depolarization ofV m. The enhanced Cl− conductance may lead to KCl extrusion and hence regulatory volume decrease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253833
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  • 7
    Electronic Resource
    Electronic Resource
    Ca2+- and swelling-induced activation of ion conductances in bronchial epithelial cells (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 597-603 
    Details
    ISSN: 1432-2013
    Keywords: Cl− conductance ; K+ conductance ; ATP ; Bradykinin ; Histamine ; Bronchial epithelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to examine Ca2+-dependent and cell-swelling-induced ion conductances in a polarized bronchial epithelial cell line (16HBE14o-). Whole-cell currents were measured in fast and slow whole-cell patch-clamp experiments in cells grown either on filters or on coated plastic dishes. In addition the transepithelial voltage (V te) and resistance (R te) were measured in confluent monolayers. Resting cells had a membrane voltage (V m) of −36±1.1 mV (n=137) which was mainly caused by K+ and Cl− conductances and to a lesser extent by a Na+ conductance. V te was apical-side-negative after stimulation. Equivalent short-circuit current (I sc = V te/R te) was increased by the secretagogues histamine (0.1 mmol/l), bradykinin (0.1–10 μmol/l) and ATP (0.1–100 μmol/l). The histamine-induced I sc was blocked by either basolateral diphenhydramine (0.1 mmol/l, n=4) or apical cimetidine (0.1 mmol/l, n=4). In fast and slow whole-cell recordings ATP and bradykinin primarily activated a transient K+ conductance and hyperpolarized V m. This effect was mimicked by the Ca2+ ionophore ionomycin (1 μmol/l, n=11). Inhibition of the bradykinin-induced I sc by the blocker HOE140 (1 μmol/l, n=3) suggested the presence of a BK2 receptor. The potency sequence of different nucleotide agonists on the purinergic receptor was UTP ≈ ATP 〉 ITP 〉 GTP ≈ CTP ≈ [β,γ-methylene] ATP ≈ 2-methylthio-ATP = 0 and was obtained in I sc measurements and patch-clamp recordings. This suggests the presence of a P2u receptor. Hypotonic cell swelling activated both Cl− and K+ conductances. The Cl− conductance was only slightly inhibited by 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (0.5 mmol/ l, n=3). These data indicate that 16HBE140- bronchial epithelial cells, which are known to express high levels of cystic fibrosis transmembrane conductance regulator protein, form a secretory epithelium. While hypotonic cell swelling activates both K+ and Cl− channels, the Ca2+-induced Cl− secretion is due mainly to activation of basolateral K+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374583
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  • 8
    Electronic Resource
    Electronic Resource
    CAMP-dependent activation of ion conductances in bronchial epithelial cells (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 590-596 
    Details
    ISSN: 1432-2013
    Keywords: Cl− channels ; Histamine ; Forskolin ; Isoproterenol ; CFTR ; Bronchial epithelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cAMP-dependent activation of Cl− channels was studied in a bronchial epithelial cell line (16HBE14o-) in fast and slow whole-cell, and cell-attached patch-clamp experiments. The cells are known to express high levels of cystic fibrosis transmembrane conductance regulator mRNA and protein. Isoproterenol, forskolin and histamine (all 10 μmol/l) reversibly and significantly depolarized the membrane voltage (V m) and increased the whole-cell Cl− conductance significantly by 34.0±0.9 (n=3), 18.1±2.7 (n=50), and 25±4.5 (n=37) nS respectively. The effect of histamine was blocked by cimetidine (10 μmol, n=5) but not by diphenhydramine (10 μmol/l, n=4), which suggests binding of histamine to H2 receptors. The forskolin-induced current was not inhibited significantly by 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (0.5 mmol/l, n=9) nor glibenclamide (10 μmol/l, n=3) and had an anion-permeability sequence of Cl−= Br−〉I− (n=9). In cell-attached recordings forskolin (10 μmol/l) increased the conductance of the patched membrane from 65.5±13.6 pS to 150.8±33.2 pS (n=30). Although the conductance was increased significantly, clear ion-channel events occurring in parallel with the current activation were not detected in the cell attached membrane. In 4 out of 30 cell-attached recordings single-channel currents were observed. These channels, with a single-channel conductance of about 6 pS, were already active before forskolin was added. No effect of forskolin on the channel amplitude, open probability or kinetics of these channels was observed. From these data we conclude that the cAMP-induced conductance increase in 16HBE14o-cells can be correlated with the activation of very small and not resolvable (probably less than 2 pS) Cl− channels rather than with the activation of channels with a conductance of 6–10 pS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374582
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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Isolated perfused rabbit colon crypts: stimulation of Cl− secretion by forskolin (1993)
    Springer
    Pflügers Archiv 425 (1993), S. 373-380 
    Details
    ISSN: 1432-2013
    Keywords: Isolated perfused colon crypt ; Basolateral membrane voltage ; Cl− conductance ; Forskolin ; Loop diuretics ; Cl− secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to characterize ion conductances and carrier mechanisms of isolated in vitro perfused rabbit colonic crypts. Crypts were isolated from rabbit colon mucosa and mounted on a pipette system which allowed controlled perfusion of the lumen. In non-stimulated conditions basolateral membrane voltage (V b1) was −65±1 mV (n=240). Bath Ba2+ (1 mmol/ l) and verapamil (0.1 mmol/l) depolarized V b1 by 21±2 mV (n=7) and 31±1 (n=4), respectively. Lowering of bath Cl− concentration hyperpolarized V b1 from −69±3 to −75±3 mV (n=9). Lowering of luminal Cl− concentration did not change V b1. Basolateral application of loop diuretics (furosemide, piretanide, bumetanide) had no influence on V b1 in non-stimulated crypts. Forskolin (10−6 mol/l) in the bath depolarized V b1 by 29±2 mV (n=54) and decreased luminal membrane resistance. In one-third of the experiments a spontaneous partial repolarization of V b1 was seen in the presence of forskolin. During forskolin-induced depolarization basolateral application of loop diuretics hyperpolarized V b1 significantly and concentration dependently with a potency sequence of bumetanide 〉 piretanide ≥ furosemide. Lowering bath Cl− concentration hyperpolarized V b1. Lowering of luminal Cl− concentration from 120 to 32 mmol/l during forskolin-induced depolarization led to a further depolarization of Vb1 by 7±2 mV (n=10). We conclude that Vb1 of rabbit colonic crypt cells is dominated by a K+ conductance. Stimulation of the cells by forskolin opens a luminal Cl− conductance. Basolateral uptake of Cl− occurs via a basolateral Na+ : 2Cl− : K+ cotransport system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374861
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