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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 941 (1988), S. 217-224 
    ISSN: 0005-2736
    Keywords: (MDCK cell) ; Acetylcholine ; Atropine ; Calcium ; Membrane potential ; Microelectrode ; Potassium conductance
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 1069 (1991), S. 165-170 
    ISSN: 0005-2736
    Keywords: Calcium ; Cell membrane potential ; Clonidine ; Epinephrine ; Patch clamp ; intracellular ; α"2-Adrenoceptor agonist
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 234 (1988), S. 263-266 
    ISSN: 0014-5793
    Keywords: (MDCK cell) ; ATP ; Acetylcholine ; Bradykinin ; Epinephrine ; Membrane potential ; Pertussis toxin ; Serotonin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 408 (1987), S. 584-591 
    ISSN: 1432-2013
    Keywords: Outward K channel ; Epinephrine ; Patch-clamp ; MDCK-cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Patch-clamp recordings were used to study the epinephrine dependent activation of ion channels in the cell membrane of cultured subconfluent renal epithelial (MDCK) cells. The patch-current was dominated by two populations of K channels. The spontaneously active population of K channels shows an inward rectifying behavior. Addition of epinephrine to the cell exterior, after the patchpipette had been sealed to the cell membrane, increased the open probability of the inward rectifying K channel and shifted the membrane potential in the hyperpolarizing direction. The epinephrine induced hyperpolarization occurs in the range of seconds and is caused by activation of outward-rectifying K channels. The outward-rectifying K channel could not be observed under control conditions. Epinephrine activated channels always appeared in clusters of four to nine channels. Both populations of K channels are modulated in their open probability by cytoplasmic free calcium and voltage.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 407 (1986), S. 258-263 
    ISSN: 1432-2013
    Keywords: MDCK-cells ; Microelectrodes ; Cell membrane potential ; Potassium conductance ; Sodium ; Calcium ; Barium ; Amiloride ; A23187
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In incompletely confluent madin Darby canine kidney cells continuous measurements of the potential difference across the cell membrane (PD) were made with conventional microelectrodes during rapid changes of extracellular sodium and/or calcium concentration. During control conditions PD averages −50.6±0.7 mV. Reduction of extracellular sodium concentration from 131.8 to 17.8 mmol/l leads to a reversible hyperpolarization of the cell membrane to −65.3±1.1 mV. This hyperpolarization is not significantly reduced by omission of glucose or presence of amiloride (1 mmol/l) in the perfusates. Instead, 1 mmol/l amiloride depolarizes the cell membrane by +5.2±0.4 mV. 1 mmol/l barium depolarizes the cell membrane to −31.3±1.1 mV. Step increases of extracellular potassium concentration from 5.4 to 10 and 20 mmol/l depolarize the cell membrane by +5.5±0.5 mV and +16.5±1.8 mV respectively. In the presence of barium, the depolarizing effect of increasing extracellular potassium concentration and of amiloride is almost abolished. Reduction of extracellular sodium concentration in the presence of barium, however, leads to a transient hyperpolarization of the cell membrane. During this transient hyperpolarization, increasing extracellular potassium concentration depolarizes the cell membrane despite the continued presence of barium. Omission of extracellular calcium (EDTA) depolarizes the cell membrane by +36.7±3.2 mV. In the absence of extracellular calcium, the hyperpolarizing effect of reduced extracellular sodium concentration is markedly reduced (−4.5±1.2 mV). 2 μmol/l A23187 in the presence of extracellular calcium hyperpolarizes the cell membrane to −72.5±0.6 mV. In conclusion, reduction of extracellular sodium concentration increases the potassium conductance of the cell membrane, possibly by increasing intracellular calcium activity via an influence on the sodium/calcium-exchange.
    Type of Medium: Electronic Resource
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