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  • 1
    Electronic Resource
    Electronic Resource
    Effects of serotonin on electrical properties of Madin-Darby canine kidney cells (1988)
    Springer
    Pflügers Archiv 411 (1988), S. 394-400 
    Details
    ISSN: 1432-2013
    Keywords: MDCK-cells ; Intracellular microelectrodes ; Cell membrane potential ; Potassium-conductance ; 5-Hydroxytryptamine (5-HT) ; Barium ; Methysergide ; ICS 205-930 ; Ketanserin ; Phentolamine ; Extracellular calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study has been performed to test for the influence of serotonin on the potential difference across the cell membrane (PD) of Madin-Darby canine kidney (MDCK)-cells. Under control conditions PD averages −48.6±0.6 mV (n=98). Increasing extracellular potassium concentration from 5.4 to 10 and 20 mmol/l depolarizes the cell membrane by +6.3±0.6 mV (n=6) and +14.1±1.0 mV (n=12), respectively. The cell membrane is transiently hyperpolarized to −67.8±0.8 mV (n=63) by 1 μmol/l serotonin. In the presence of serotonin, increasing extracellular potassium concentration from 5.4 to 20 mmol/l depolarizes the cell membrane by +26.4±1.0 mV (n=11). 1 mmol/l barium depolarizes the cell membrane by +15.7±1.3 mV (n=17) and abolishes the effect of step increases of extracellular potassium concentration from 5.4 to 10 mmol/l. In the presence of barium, serotonin leads to a transient hyperpolarization by −26.3±1.0 mV (n=16). During this transient hyperpolarization, the cell membrane is sensitive to extracellular potassium concentration despite the continued presence of barium. 10 μmol/l methysergide hyperpolarize the cell membrane by −7.2±2.0 mV (n=6). In the presence of 10μmol/l methysergide, the effect of serotonin is virtually abolished (+0.4±0.9 mV,n=6). 1 μmol/l ketanserin, a 5-HT2 receptor blocking agent, ICS 205-930, a 5-HT3 receptor blocking agent, and phentolamine, an unspecific α-receptor blocking agent, do not significantly modify the effect of serotonin. In the nominal absence of extracellular calcium, the effect of serotonin is markedly reduced. In conclusion, serotonin hyperpolarizes MDCK-cells by increasing apparent potassium conductance. This effect is transmitted by 5-HT1 receptors and depends on extracellular calcium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00587718
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanism of intracellular calcium oscillations in fibroblasts expressing the ras oncogene (1992)
    Springer
    Pflügers Archiv 420 (1992), S. 208-212 
    Details
    ISSN: 1432-2013
    Keywords: Ras oncogene ; Bradykinin ; NIH fibroblasts ; Intracellular calcium oscillations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In NIH fibroblasts expressing the ras oncogene bradykinin leads to sustained, calcium-dependent oscillations of cell membrane potential by oscillating activity of calcium sensitive potassium channels. The present study has been performed to further analyse the underlying mechanisms. In cells expressing the oncogene, but not in NIH fibroblasts not expressing the oncogene, bradykinin elicits calcium oscillations, which are detected by fura-2 fluorescence and amplified by a decrease of extracellular sodium activity. These calcium oscillations are dependent on the presence of extracellular calcium and are inhibited by lanthanum ions. It is concluded that in cells expressing the ras oncogene, bradykinin activates lanthanum sensitive calcium entry from the extracellular space. Ras oncogene expression leads to enhanced bradykinin-induced formation of both, 1, 4, 5 inositoltrisphosphate and 1, 3, 4, 5 inositoltetrakisphosphate, an effect probably accounting for the oscillations of intracellular calcium activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374992
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  • 3
    Electronic Resource
    Electronic Resource
    Further analysis of ATP-mediated activation of K+ channels in renal epitheloid Madin Darby canine kidney (MDCK) cells (1991)
    Springer
    Pflügers Archiv 418 (1991), S. 551-555 
    Details
    ISSN: 1432-2013
    Keywords: MDCK cells ; K+ channels ; ATP activation ; Phorbol ester ; Pertussis toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract ATP activates K+ channels by increasing intracellular calcium activity in Madin Darby canine kidney (MDCK) cells. The present study has been performed to test for the involvement of G-proteins and of protein kinase C in the intracellular transmission of these effects. To this end, the effect of ATP on intracellular calcium and K+ channel activity has been studied in cells pretreated with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and/or pertussis toxin. The ATP-induced increase of intracellular calcium is not significantly affected by pretreatment with pertussis toxin, is significantly blunted by pretreatment with TPA and is abolished by pretreatment with both pertussis toxin and the phorbol ester. The ATP activation of K+ channels is similarly blunted by pretreatment with TPA, but is not abolished by pretreatment with both the phorbol ester and pertussis toxin. Furthermore, the ATP-induced hyperpolarization is not abolished in cells pretreated with both pertussis toxin and TPA. In those cells, ATP may activate K+ channels by calcium-independent mechanisms or lead to localized increases of intracellular calcium sufficient to activate the K+ channels but escaping detection with fura-2 fluorescence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370570
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  • 4
    Electronic Resource
    Electronic Resource
    Altered cell volume regulation in ras oncogene expressing NIH fibroblasts (1992)
    Springer
    Pflügers Archiv 420 (1992), S. 424-427 
    Details
    ISSN: 1432-2013
    Keywords: Cell volume regulation ; Ras oncogene ; Na+/H+ Exchanger ; Na+, K+,2Cl− Cotransporter ; Dimethylamiloride ; Furosemide ; Quinidine ; Bumetanide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Expression of the Ha-ras oncogene has been reported to stimulate the dimethylamiloride sensitive Na+/H+ exchanger and Na+, K+, 2Cl− cotransport, both transport systems which are involved in cell volume regulation. The present study has been performed to test for an influence of ras oncogene expression on cell volume regulation in NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ ras). As controls served NIH 3T3 fibroblasts not expressing the ras oncogene (− ras). In isotonic extracellular fluid, the cell volume of + ras cells (2.70±0.08 pl) is significantly greater than the cell volume of −ras cells (2.04±0.10 pl). Both, + ras and − ras cells exhibit a regulatory cell volume increase in hypertonic extracellular fluid and a regulatory cell volume decrease in hypotonic extracellular fluid. The regulatory cell volume decrease is inhibited by 1 mmol/l quinidine and barium, the regulatory cell volume increase is inhibited in − ras and + ras cells by dimethyl-amiloride (100 μmol/l) and, only in + ras cells, by furosemide (100 μmol/l) and bumetanide (10 μmol/l). In conclusion, expression of the ras oncogene leads to a shift of the set point for cell volume regulation to greater cell volumes, which may contribute to the activation of the Na+/H+ exchanger and Na+, K+, 2Cl− cotransport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374615
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  • 5
    Electronic Resource
    Electronic Resource
    Cell shrinkage stimulates bradykinin-induced cell membrane potential oscillations in NIH 3T3 fibroblasts expressing the ras-oncogene (1993)
    Springer
    Pflügers Archiv 423 (1993), S. 221-224 
    Details
    ISSN: 1432-2013
    Keywords: Cell volume ; Intracellular pH ; ras oncogene ; Calcium oscillations ; Cell membrane potential ; Bradykinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ras) bradykinin leads to sustained oscillations of cell membrane potential due to oscillations of intracellular Ca2+ with subsequent activation of Ca2+-sensitive K+ channels. In cells not expressing the oncogene (-ras), bradykinin leads only to a single transient hyperpolarization of the cell membrane. The present study has been performed to elucidate the possible interaction of cell volume, intracellular pH and bradykinin-induced oscillations of the cell membrane potential. Bradykinin leads to cell shrinkage and intracellular alkalinization of both +ras cells and −ras cells. Inhibition of Na+/H+ exchanger by HOE 694 abolishes the bradykinin-induced alkalinization but does not significantly interfere with the bradykinin-induced oscillations of cell membrane potential. In contrast, prevention of bradykinin-induced cell shrinkage by simultaneous reduction of extracellular osmolarity blunts the oscillations. Thus, cell shrinkage stimulates bradykinin-induced oscillations of cell membrane potential. On the other hand, cell shrinkage alone does not elicit oscillations unless, in addition, Ca2+ entry is stimulated by ionomycin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374398
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of inhibitors and ion substitutions on oscillations of cell membrane potential in cells expressing the RAS oncogene (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 416-424 
    Details
    ISSN: 1432-2013
    Keywords: ras oncogene ; Cell membrane potential ; Ca2+ channels ; K+ channels ; Bradykinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies revealed that in NIH fibroblasts expressing the ras oncogene but not in other NIH fibroblasts, bradykinin leads to sustained, calcium dependent oscillations of cell membrane potential by repetitive activation of calcium-sensitive K+ channels. The present study has been performed to test for ion and inhibitor sensitivity of these oscillations. Both, Lys-bradykinin (kallidin) and bradykinin, but not any shorter peptide tested, maintained the oscillations. The oscillations are abolished in the presence of the K+ channel blocker barium (10 nmol/l). The amplitude but not the frequency of the oscillations is dependent on the extracellular potassium concentration. The oscillations are not dependent on the presence of extracellular sodium, bicarbonate or chloride. The oscillations are abolished in the absence of extracellular calcium and their frequency is significantly decreased at reduced extracellular calcium (to 0.2 mmol/l). The oscillations are not inhibited by acute administration of ouabain (0.1 mmol/l), by dimethylamiloride (100 μmol/l), furosemide (1 mmol/l) and hydrochlorothiazide (100 μmol/l), by cobalt (100 μmol/l), zinc (100 μmol/l), gadolinium (100 μmol/l), verapamil (10 μmol/l) and diltiazem (10 μmol/l), but are abolished in the presence of 100 μmol/l lanthanum, 1 mmol/l cadmium, 10 μmol/l nifedipine, 25 μmol/l SK & F 96365 and 200 μmol/l TMB-8. Stimulation of calcium entry by 10 μmol/l ionomycin is frequently followed by oscillations of cell membrane potential even in the absence of bradykinin. In conclusion, in cells expressing the ras oncogene bradykinin leads to sustained activation of calcium channels at the cell membrane, which cause oscillations of the cell membrane potential by triggering intracellular calcium release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370251
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  • 7
    Electronic Resource
    Electronic Resource
    Cellular mechanisms of ATP-induced hyperpolarization in renal epitheloid MDCK-cells (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 147 (1991), S. 68-75 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Previous studies have shown that ATP enhances intracellular calcium concentration and activates potassium channels in Madin Darby canine kidney (MDCK)-cells, thus leading to hyperpolarization of the cell membrane. The present study has been performed to elucidate the intracellular mechanisms involved. To this end, the effects of ATP on the potential difference across the cell membrane (PD), on formation of inositol phosphates, and on intracellular calcium concentration (Cai) have been analyzed in cells without or with pretreatment with pertussis toxin or 12-O-tetradecanoyl phorbol 13-acetate diester (TPA). In untreated cells, ATP leads to a sustained hyperpolarization and an increase of inositol 1,4,5-tris-phosphate (IP3), inositol 1,3,4,5-tetrakisphosphate (IP4), and Cai. In the absence of extracellular calcium, the effect of ATP on PD and Cai is only transient. In cells pretreated with pertussis toxin, the effect of ATP on inositol trisphosphate is almost abolished, but ATP still leads to an increase of PD and Cai, which is sustained in the presence, and transient in the absence, of extracellular calcium. In cells pretreated with TPA, the effect of ATP on inositol trisphosphate is reduced and the effect on Cai blunted; but ATP still leads to a hyperpolarization of the cell membrane, which is sustained in the presence, and transient in the absence, of extracellular calcium. The observations indicate that ATP activates phospholipase C by a phorbol ester and pertussis toxin sensitive mechanism. In addition, ATP enhances Cai by pertussis toxin insensitive mechanisms allowing recruitment of calcium from both, extracellular fluid and intracellular stores. Calcium then activates the potassium channels and thus leads to the hyperpolarization of the cell membrane.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041470110
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of trifluoperazine on renal epitheloid madin-darby canine kidney cells (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 148 (1991), S. 314-319 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Following exposure to a number of hormones, the cell membrane in Madin-Darby Canine Kidney (MDCK) cells is hyperpolarized by increase of intracellular calcium activity. The present study has been performed to elucidate the possible role of calmodulin in the regulation of intracellular calcium activity and cell membrane potential. To this end trifluoperazine has been added during continuous recording of cell membrane potential or intracellular calcium. Trifluoperazine leads to a transient increase of intracellular calcium as well as a sustained hyperpolarization of the cell membrane by activation of calcium sensitive K+ channels. Half-maximal effects are observed between 1 and 10 μmol/L trifluoperazine. A further calmodulin antagonist, chlorpromazine, (50 μmol/L), similarly hyperpolarizes the cell membrane. The effects of trifluoperazine are virtually abolished in the absence of extracellular calcium. Pretreatment of the cells with either pertussis toxin or phorbolester TPA does not interfere with the hyperpolarizing effect of trifluoperazine. In conclusion, calmodulin is apparently involved in the regulation of calcium transfer across the cell membrane but not in the stimulation of K+ channels by intracellular calcium.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041480218
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