Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Cl− conductance  (11)
  • 1
    Electronic Resource
    Electronic Resource
    Characterization of human sweat duct chloride conductance by chloride channel blockers (1987)
    Springer
    Pflügers Archiv 408 (1987), S. 511-514 
    Details
    ISSN: 1432-2013
    Keywords: Human sweat duct ; Cl− conductance ; Cl− channel blockers ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To characterize the chloride conductance of human sweat duct the effect of various analogues of diphenylamine-2-carboxylate was investigated on the transepithelial potential difference (PDT) and resistance (R T ) of isolated microperfused sweat ducts. Although the most powerful analogues which block Cl− channels in various secretory and absorptive epithelia were ineffective, a number of analogues (in particular Cl substituted ones) were found which at high concentrations significantly and reversibly increased PDT andR T . The data suggest that the main chloride conductance pathway of sweat duct epithelium resides in the cell membranes rather than in the tight junctions. In addition the different blocking spectra of the chloride conductances of sweat duct and tracheal epithelium (Welsh MJ, Science 232:1648, 1986) suggest that the combined impairment of both conductances in cystic fibrosis does not result from a molecular defect in the Cl− channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585077
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Transmitter-induced changes of the membrane voltage of HT29 cells (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 224-229 
    Details
    ISSN: 1432-2013
    Keywords: Cl− conductance ; HT29 ; P2 receptor ; Colon ; Cl− secretion ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The colonic carcinoma cell line HT29 was used to examine the influence of agonists increasing cytosolic cAMP and Ca2+ activity on the conductances and the cell membrane voltage (V m). HT29 cells were grown on glass cover-slips. Cells were impaled by microelectrodes 4–10 days after seeding, when they had formed large plaques. In 181 impalements V m was −51±1 mV. An increase in bath K+ concentration from 3.6 mmol/l to 18.6 mmol/l or 0.5 mmol/l Ba2+ depolarized the cells by 10±1 mV (n=49) or by 9±2 mV (n=3), respectively. A decrease of bath Cl− concentration from 145 to 30 mmol/l depolarized the cells by 11±1 mV (n=24). Agents increasing intracellular cAMP such as isobutylmethylxanthine (0.1 mmol/l), forskolin (10 μmol/l) or isoprenaline (10 μmol/l) depolarized the cells by 6±1 (n=13), 15±3 (n=5) and 6±2 (n=3) mV, respectively. In hypoosmolar solutions (225 mosmol/l) cells depolarized by 9±1 mV (n=6). Purine and pyrimidine nucleotides depolarized the cells dose-dependently with the following potency sequence: UTP 〉 ATP 〉 ITP 〉 GTP 〉 TIP 〉 CTP = 0. The depolarization by ATP was stronger than that by ADP and adenosine. The muscarinic agonist carbachol led to a sustained depolarization by 27±6 mV (n=5) at 0.1 mmol/l, and to a transient depolarization by 12±4 mV (n=5) at 10 μmol/l. Neurotensin depolarized with a half-maximal effect at around 5 nmol/l. The depolarization induced by nucleotides and neurotensin was transient and followed by a hyperpolarization. We confirm that HT29 cells possess Cl−- and K+-conductive pathways. The Cl− conductance is regulated by intracellular cAMP level, cytosolic Ca2+ activity, and cell swelling. The K+ conductance in HT29 cells is regulated by intracellular Ca2+ activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374831
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Forskolin and PMA pretreatment of HT29 cells alters their chloride conductance induced by cAMP, Ca2+ and hypotonic cell swelling (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 76-83 
    Details
    ISSN: 1432-2013
    Keywords: HT29 ; CFPAC-1 ; Cl− secretion ; CFTR ; CF ; Cl− conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract HT29 cells were preincubated with forskolin (10−5 mol/l, FORHT) or phorbol 12-myristate 13-acetate (PMA) (10−7 mol/l, PMAHT) for 20 h, which has been shown previously and is also shown here, to upregulate and downregulate, respectively, the expression of the cystic fibrosis transmembrane conductance regulator (CFTR). CFPAC-1 cells underwent the same protocols. HT29 cells were examined by slow (SWC) and fast (FWC) whole-cell patch-clamp techniques. The results of SWC and FWC were indistinguishable and were pooled. CFPAC-1 cells were examined with FWC. The membrane voltage (V) of FORHT was -41.8±1.4 mV (n=77) and that of PMAHT was -43.6±2.4 mV (n=76). The conductance (G) of FORHT (9.4 ±0.9 nS, n=77) was significantly larger than that of PMAHT (3.7±0.4 nS, n=76). Acute application of forskolin (10−5 mol/l, FOR) plus 0.5 mmol/l 8-(4-chlorophenylthio)-cAMP (cAMP) depolarized V by 12 (FORHT) and 8 (PMAHT) mV, respectively. The acute increase of G by FOR plus cAMP was by 7.6±1.9 nS for FORHT (n=22) and only 2.2±1 nS for PMAHT (n=13). ATP (10−4 mol/l) depolarized V in both types of cells. It enhanced G by 16.7±4.1 nS in FORHT (n=14) and significantly less (by 5.5±1.2nS, n=14) in PMAHT. Also the G increase lasted longer in FORHT. Neurotensin (NT, 10−8 mol/l) also had a stronger and longer lasting effect in FORHT. Exposure to hypotonic bath solution (160 mosmol/l) depolarized V in both types of cells. The increase in G was by 15±2.2 nS in FORHT (n=18) and by 11±1.3 nS in PMAHT (n=23). After being returned to the normotonic media, the decline of G to the control value was delayed in FORHT when compared to PMAHT. Ionomycin (10−7 mol/l) increased G significantly more (to 47±8.5 nS, n=13) in FORHT when compared to PMAHT (to 28±4 nS, n=13). The present data indicate that a 20-h exposure of HT29 cells to FOR versus PMA alters markedly the CFTR concentration. The cells with high CFTR (FORHT) when compared to those with low CFTR (PMAHT) differ not only in their acute G response to cAMP, but also in that to ATP, NT, hypotonic cell swelling, and ionomycin. In contrast, the same pretreatment of CFPAC-1 cells did not alter the G changes induced by ionomycin or hypotonic cell swelling. These results indicate that changes in CFTR expression correlate with the Cl− conductances induced by cAMP, Ca2+ and hypotonic cell swelling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374754
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Effect of bradykinin and histamine on the membrane voltage, ion conductances and ion channels of human glomerular epithelial cells (hGEC) in culture (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 137-144 
    Details
    ISSN: 1432-2013
    Keywords: Human glomerular epithelial cells ; Bradykinin ; Histamine ; Nystatin patch clamp technique ; K+ conductance ; Maxi K+ channel ; Cl− conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of bradykinin (BK) and histamine (Hist) on the membrane voltage (V m), ion conductances and ion channels of cultured human glomerular epithelial cells (hGEC) were examined with the nystatin patch clamp technique. Cells were studied between passage 3 and 20 in a bath rinsed with Ringer-like solution at 37°C. The mean value of V m was −41±0.5 mV (n=189). BK (10−6 mol/l, n=29) and Hist (10−5 mol/l, n= 55) induced a rapid transient hyperpolarization by 15±1 mV and 18±1 mV, respectively. The hyperpolarization was followed by a long lasting depolarization by 6±1 mV (BK 10−6 mol/l) and 7±1 mV (Hist 10−5 mol/l). The ED50 was about 5×10−8 mol/l for BK and 5×10−7 mol/l for Hist. In the presence of both agonists, increases of outward and inward currents were observed. A change in the extracellular K+ concentration from 3.6 to 30 mmol/l depolarized V m by 8±1 mV and completely inhibited the hyperpolarizing effect of both agents (n=11). Reduction of extracellular Cl− concentration from 145 to 30 mmol/l led to a depolarization by 2 ±1 mV (n=25). In 30 mmol/l Cl− the depolarizations induced by BK (10−7 mol/l) and Hist (10−6 mol/l) were augmented to 9±2 mV (n=14) and to 10±2 mV (n=11), respectively. Ba2+ (5 mmol/l) depolarized V m by 19±5 mV (n=6) and completely inhibited the hyperpolarization induced by BK (10−6 mol/l, n=3) and reduced that of Hist (10−5 mol/l) markedly (n=3). Preincubation with the K+ channel blocker charybdotoxin (1–10 nmol/l) for 3 min had no significant effect on V m, but reduced markedly the BK(10−6 mol/l, n=11) and Hist-(10−5 mol/l, n=6) induced hyperpolarizations. In 10 out of 31 experiments in the cell attached nystatin patch configuration big K+ channels with a conductance $$(g_{K^ + } )$$ of 247±17 pS were found. The open probability of these K+ channels was increased 3- to 5-fold during the hyperpolarization induced by BK (10−7 mol/l) or Hist (10−5 mol/l, both n= 4). In excised inside/out patches this K+ channel had a mean conductance of 136±8.5 pS (n=10, clamp voltage 0 mV). The channel was outwardly rectifying and its open probability was increased when Ca2+ on the cytosolic side was greater than 0.1 μmol/l. The data indicate that BK and Hist activate a $$(g_{K^ + } )$$ and a $$g_{Cl^ - } $$ in hGEC. The hyperpolarization is induced by the activation of a Ca2+-dependent maxi K+ channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374604
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    The effect of secretagogues on ion conductances of in vitro perfused, isolated rabbit colonic crypts (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 494-502 
    Details
    ISSN: 1432-2013
    Keywords: Cl− secretion ; cAMP ; K+ conductance ; Cl− conductance ; Diarrhoea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Several secretagogues were used in this study, including those which enhance intracellular cyclic adenosine monophosphate (cAMP) production, as well as others which elevate intracellular Ca2+ activity and are known to increase Cl− secretion in the intact colon and in colonic carcinoma cell lines. They were examined with respect to their effects on electrophysiological properties in isolated rabbit distal colonic crypts. Crypts were dissected manually and perfused in vitro. Transepithelial voltage (V te), transepithelial resistance (R te), membrane voltage across the basolateral membrane (V bl), and fractional basolateral membrane resistance (FR bl), were estimated. Basolateral prostaglandin E2 (PGE2, ⩾0.1 μmol/l), vasoactive intestinal peptide (VIP, 1 nmol/l) and adenosine (0.1 mmol/l) induced an initial depolarisation and a secondary partial repolarisation of (V bl). In the case of adenosine, the initial depolarization of (V bl) was by 31±2 mV (n=47).R te fell significantly from 16.4±3.6 to 14.2±3.7 Ω·cm2 (n= 6), andFR blincreased significantly from 0.11±0.02 to 0.51±0.10 (n=6). In the second phase the repolarisation of (V bl) amounted 11±2 mV (n=47) and a steadystate (V bl) of −51±2 mV (n=47) was reached.R te fell further and significantly to a steady-state value of 12.4±3.8 Ω·cm2 (n=6) andFR bl fell significantly to 0.42±0.13 (n=6). In 30% of the experiments, a transient hyperpolarisation of (V bl) by 8±2 mV (n=14) was seen during wash out of adenosine. In the presence of adenosine, but not under control conditions, lowering of luminal Cl− concentration from 120 to 32 mmol/l depolarised (V bl) significantly by 8±1 mV (n=9). Basolateral ATP and ADP (0.1 mmol/l) led to a short initial depolarisation followed by a sustained and significant hyperpolarisation by 6±2 mV (n=27) and 5±4 mV (n=8), respectively. Carbachol (CCH) hyperpolarised (V bl) in a concentration-dependent manner. At 100 μmol/l (bath) the hyperpolarisation was by 14±2 mV (n=11) andFR bl fell slightly. Neurotensin (⩾10 nmol/l), isoproterenol (⩾10 μmol/l) and uridine 5′-triphosphate (UTP, 0.1 mmol/l) had no effect. It is concluded that PGE2, VIP and adenosine upregulate sequentially a luminal Cl− conductance and a basolateral K+ conductance by increasing intracellular cAMP concentration. Ca2+ mobilising hormones such as ATP, ADP, and CCH increase the basolateral K+ conductance, while the effect on luminal Cl− conductance appears to be very limited.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00704154
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...