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  • 1
    Electronic Resource
    Electronic Resource
    Potassium conductance of smooth muscle cells from rabbit aorta in primary culture (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 57-68 
    Details
    ISSN: 1432-2013
    Keywords: Vascular smooth muscle cell ; K+ conductance ; Big Ca2+-dependent K+ channel ; Patch clamp ; Verapamil ; Protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vascular smooth muscle cells were obtained from rabbit aorta and were studied in primary culture on days 1–7 after seeding with electrophysiological techniques. In impalement experiments a mean membrane potential difference (PD) of −50±0.3 mV (n=387) was obtained with Ringer-type solution in the bath. PD was depolarized by 6±0.3 mV (n=45) and 16±2 mV (n= 5) when the bath K+ concentration was increased from the control value of 3.6 mmol/l to 13.6 and 23.6 mmol/l, respectively. Ba2+ (0.1–1 mmol/l) depolarized PD. Tetraethylammonium (TEA, 10 mmol/l) depolarized PD only slightly but significantly. Verapamil (0.1 mmol/l) and charybdotoxin (10 nmol/l) had no effect on PD. The conductance properties of these cells were further examined with the patch-clamp technique. K+ channels were spontaneously present in cell-attached patches. When the pipette was filled with 145 mmol/l KCl, a mean conductance (g K) of 209.6±4.6 mV (n=17) was read from the current/voltage curves at a clamp voltage (V c) of 0 mV. After excision K+ channels were found in 129 patches with inside-out and in 50 with outside-out configuration. With KCl on one and NaCl on the other side the mean g K at a V c of 0 mV was 134.6±3.9 pS (n=179). The mean permeability was 0.89±0.03×10−12 cm3/s. With symmetrical KCl solution the mean g K was 227±6 pS (n=17). The conductance sequence was g K≫ g Rb= g Cs=g Na=0. TEA blocked dose-dependently only from the outside.(1–10 mmol/l). Lidocaine (5 mmol/l) quinidine (0.01–1 mmol/l) and quinine (0.01–1 mmol/l) blocked from both sides. Charybdotoxin (0.5–5 nmol/l) blocked only from the extracellular side. Ba2+ blocked from the cytosolic side and the inhibition was increased by depolarization and reduced by hyperpolarization. At a V c of 0 mV a half-maximal inhibition (IC50) of 2 μmol/l was obtained. Verapamil and diltiazem blocked from both sides, verapamil with an IC50 of 2 μmol/l and diltiazem with an IC50 of 10 μmol/l. The open probability of this channel was increased by Ca2+ on the cytosolic side at activities 〉 0.1 μmol/l. Half-maximal activation occurred at Ca2+ activities exceeding 1 μmol/l. The present data indicate that the vascular smooth muscle cells of rabbit aorta in primary culture possess a K+ conductance. In excised patches only a maxi K+ channel was detected. This channel has properties different from the macroscopic K+ conductance. Hence, it is likely that the K+ conductance of the intact cell is dominated by yet another and thus far not detected K+ channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373748
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of depolarizing and hyperpolarizing agents on the membrane potential difference of primary cultures of rabbit aorta vascular smooth muscle cells (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 69-75 
    Details
    ISSN: 1432-2013
    Keywords: Vascular smooth muscle cells ; Membrane potential ; Cromakalim ; Glibenclamide ; K+ channels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vascular smooth muscle cells of rabbit aorta were enzymatically dispersed, kept in primary culture, and studied between days 1 and 7 in a bath rinsed with Ringer-like solution at 37°C. The electrical membrane potential difference (PD) was measured with microelectrodes. The mean value of PD was −50±0.4 mV (n=53). Cromakalim (BRL 34915), 1 μmol/l and 10 μmol/l, hyperpolarized the membrane potential by 9±1 mV (n=11) and 15±1 mV (n=53) respectively. Glibenclamide (10 μmol/l) abolished the hyperpolarizing effect of cromakalim (n=6). Simultaneous addition of cromakalim and glibenclamide (both 10 μmol/l, n=11) and glibenclamide itself (10 μmol/l, n=7) had no effect on PD. In patch-clamp experiments in outside-out-oriented Ca2+-sensitive K+ channels, cromakalim increased the open probability (P o) only slightly and only with a cytosolic Ca2+ activity of 1 μmol/l. In all other series cromakalim had no effect on the P o of these channels. Forskolin (10 μmol/l) hyperpolarized PD by 6±1 mV (n=13). The nucleotides UTP, ATP and ITP (10 μmol/l) depolarized PD by 12±1 mV (n=7), 8±1 mV (n=65) and 5±1 mV (n=6) respectively. GTP, [α,β-methylene]ATP and adenosine had no significant effect. Mn2+ (1 mmol/l, n=18), Ni2+ (1 mmol/l, n=13), Co2+ (1 mmol/l, n=11), Zn2+ (1 mmol/l, n=6) and the Ca2+-channel blockers verapamil and nifedipine (both 0.1 mmol/l, n=6) did not attenuate the depolarization induced by 10 μmol/l ATP. Fetal calf serum (100 ml/l, n=7) depolarized PD by 11±2 mV. This effect was not abolished by nifedipine or by replacing NaCl by choline chloride. The data indicate that PD of vascular smooth muscle cells is depolarized by P2 agonists and hyperpolarized by the K+-channel opener cromakalim. The effect of cromakalim is antagonized by glibenclamide. The effect of cromakalim is probably not mediated by the K+ channel identified in excised patches.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373749
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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