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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 19 (1987), S. S56 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 19 (1987), S. 865-874 
    ISSN: 0022-2828
    Keywords: Lidocaine ; Na channels ; Single ventricular cells ; patch clamp
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 18 (1986), S. 691-710 
    ISSN: 0022-2828
    Keywords: Beta-adrenergic receptor ; Calcium channel ; Dihydropyridine ; Ion channel ; Modulation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 19 (1987), S. 897-907 
    ISSN: 0022-2828
    Keywords: Interval strength relationship ; Laser diffractometry ; Myocardial cells ; Staircase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Molecular Cell Research 1222 (1994), S. 287-291 
    ISSN: 0167-4889
    Keywords: Calcium ion influx, receptor mediated ; Endothelial cell ; Histamine ; Intracellular calcium ion oscillation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Molecular Cell Research 1014 (1989), S. 259-262 
    ISSN: 0167-4889
    Keywords: (Guinea pig) ; Angiotensin II ; Heart muscle ; Patch clamp ; Phosphorylation ; Protein kinase C ; Sodium channel
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 1068 (1991), S. 254-256 
    ISSN: 0005-2736
    Keywords: Cardiac muscle ; Sodium ion channel ; Sodium, intracellular
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 163 (1998), S. 97-110 
    ISSN: 1432-1424
    Keywords: Key words: Patch clamp — Ca2+- and voltage-dependence — Regulatory Volume Decrease — Tamoxifen — Niflumic acid — Mg2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. A Ca2+-activated (I Cl,Ca) and a swelling-activated anion current (I Cl,vol) were investigated in Ehrlich ascites tumor cells using the whole cell patch clamp technique. Large, outwardly rectifying currents were activated by an increase in the free intracellular calcium concentration ([Ca2+] i ), or by hypotonic exposure of the cells, respectively. The reversal potential of both currents was dependent on the extracellular Cl− concentration. I Cl,Ca current density increased with increasing [Ca2+] i , and this current was abolished by lowering [Ca2+] i to 〈1 nm using 1,2-bis-(o-aminophenoxy)ethane-N,N,N′,N′-tetra-acetic acid (BAPTA). In contrast, activation of I Cl,vol did not require an increase in [Ca2+] i . The kinetics of I Cl,Ca and I Cl,vol were different: at depolarized potentials, I Cl,Ca as activated in a [Ca2+] i - and voltage-dependent manner, while at hyperpolarized potentials, the current was deactivated. In contrast, I Cl,vol exhibited time- and voltage-dependent deactivation at depolarized potentials and reactivation at hyperpolarized potentials. The deactivation of I Cl,vol was dependent on the extracellular Mg2+ concentration. The anion permeability sequence for both currents was I − 〉 Cl− 〉 gluconate. I Cl,Ca was inhibited by niflumic acid (100 μm), 5-Nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, 100 μm) and 4,4′-diisothiocyano-2,2′-stilbenedisulfonic acid (DIDS, 100 μm), niflumic acid being the most potent inhibitor. In contrast, I Cl,vol was unaffected by niflumic acid (100 μm), but abolished by tamoxifen (10 μm). Thus, in Ehrlich cells, separate chloride currents, I Cl,Ca and I Cl,vol, are activated by an increase in [Ca2+] i and by cell swelling, respectively.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1424
    Keywords: Volume regulation ; Multidrug resistance ; Cancer cells ; Chloride channels ; MDR-1 gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The characteristics of volume-activated chloride currents, drug transport function and levels of P-glycoprotein (PgP) expression were compared between two human chronic erythroleukemia cell lines: a parental (K562) cell line and a derivative obtained by vinblastine selection (K562 VBL400). Parental K562 cells showed no detectable P-glycoprotein expression, measured at the protein level (immunofluorescence labeling with monoclonal antibodies), and had very low levels of MDR-1 mRNA expression (RT-PCR analysis), when compared with levels measured in K562 VBL400. Differences in Pgp-mediated transport were estimated by comparing the rates of Fluo3 accumulation. The higher drug-transport function of K562 VBL400 cells (e.g., lower Fluo3 accumulation) correlated with their elevated levels of MDR-1. The rate of dye transport was sensitive to verapamil but was not affected by the tonicity of the extracellular medium. In contrast to the clear differences in transport function, the characteristics of chloride currents induced by cell swelling were indistinguishable between the two cell lines. Currents measured in the whole-cell configuration were outwardly rectifying, had a higher permeability to iodide than to chloride (SCN− 〉 I− 〉 Cl− 〉 gluconate), were potently blocked by NPPB and were unresponsive to verapamil. The percentage of responding cells and the mean current density were nearly identical in both cell lines. In addition, activation of the volume-sensitive current was not prevented during whole-cell recordings obtained with pipettes containing high concentration of cytotoxic drugs (vincristine or vinblastine). These results do not lend support to the previously reported association between Pgp expression and volume-sensitive chloride channels, and suggest that a different protein is responsible for this type of chloride channel in K562 cells.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1424
    Keywords: Key words: Endothelial cells — Volume-activated Cl− currents —ICln— Nucleosides — Gossypol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. We have measured the kinetic and pharmacological properties of volume-activated Cl− currents (I Cl,vol) in endothelial cells, and tried to correlate them with those of the already described volume-activated current I Cln. Both conductances show a similar permeability sequence for monovalent anions, and they are blocked by extracellular ATP. In the present report, we demonstrate by Western blot and RT-PCR that cultured endothelial cells from bovine pulmonary artery (CPAE) contain pI Cln. The expression of this protein has been shown to be closely associated with the I Cln current. I Cl,vol showed however, in contrast with I Cln, no striking inactivation at positive potentials. This property is also at variance with that of the volume-activated current related to MDR-1. Activation of I Cl,vol at potentials more negative than −80 mV was not time dependent, which excludes a major contribution of a ClC-2 related current. The antiviral nucleoside analogue AZT (3′-azido-3′-deoxythymidine) inhibited I Cl,vol by 21 ± 2.7% (n = 10), at a concentration of 100 μm. Another antiviral drug, acyclovir (ACV, 9-[(2-hydroxyethoxy)methyl]guanine) blocked I Cl,vol by 27 ± 6.2% at 100 μm (n = 11). Both blocking effects are much smaller than those reported for I Cln. The phenol derivative gossypol, which blocks I Cln-related currents, efficiently inhibited I Cl,vol in CPAE cells (67 ± 2.1% at 1 μm, n = 7, K I = 0.4 μm). The presence of pI Cln in CPAE cells and the similar qualitative pharmacological profile of I Cl,vol and I Cln support the hypothesis that pI Cln is a good molecular candidate for I Cl,vol in endothelial cells. The discrepant kinetic properties may indicate that these time-dependent currents at high positive or negative potentials are not intrinsic properties of the channels, but are caused by time-dependent depletion/accumulation phenomena due to the large amplitudes of these currents.
    Type of Medium: Electronic Resource
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