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  • 1
    ISSN: 1432-2013
    Keywords: Single smooth muscle cell ; Ca-dependent K-channel ; Patch clamp technique ; Tetraethylammonium (TEA) ; Ion channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dispersed single smooth muscle cells of rabbit portal vein were prepared by treatment with collagenase and trypsin. The muscle cells were 100–300 μm in length, 5–10 μm in maximum width and cylindrical in shape. In insideout membrane patches, two different amplitudes of ionic currents were recorded, and these single channel conductances were 273 pS (Kl-channel) and 92 pS (Ks-channel), when both sides of the membrane were exposed to 142 mM K+ solution. The channel conductances depended on concentrations of K+ on both sides of the membrane. When K+ were replaced with Na+ or Tris+, these single-channel currents were abolished. When the concentration of Ca2+ inside the membrane was greater than 10−7 M, the channel activity was enhanced but there was enhancement when Ca2+ was applied to the extracellular membrane surface, in concentrations ranging between 10−9 and 10−3 M. During application of tetraethylammonium (TEA+; 1–10 mM) to the intracellular membrane surface, amplitudes of the single-channel current of both types of the K-channel were not modified. By contrast application of TEA+ (0.1–1 mM) to the extracellular membrane surface, reduced the amplitudes of the current and increased noise levels during the open-state of the Kl-channels, but did not have such an effect on the Ks-channel. We conclude that there are at least two different Ca-dependent K-channels distributed on the smooth muscle membrane of the rabbit portal vein. TEA+ applied to the extracellular membrane surface blocks activation of the Kl-channel, but not that of the Ks-channel. These two Ca-dependent K-channels do not seem to be important for maintenance of the resting membrane potential, but do play an important role in the repolarizing stage of the Ca spikes, in the rabbit portal vein.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 294-302 
    ISSN: 1432-1912
    Keywords: Canine thoracic aorta ; PGI2 and 6-keto PGF1α ; Endothelium dependent relaxation ; PGI2-induced vasodilation ; Acetylcholine-induced vasodilation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In circular-cut strips prepared from canine thoracic aorta, acetylcholine (ACh) and A23187 relaxed endothelium-intact tissues [E(+) preparations] pre-contracted with noradrenaline or excess concentrations of K. These relaxations were associated with marked increases in the amount of 6-keto PGF1α. After removal of the endothelium [E(−) preparations] the relaxation ceased, and the amounts of 6-keto PGF1α were markedly reduced. In E(+) preparations, application of indomethacin attenuated the increase in 6-keto PGF1α induced by ACh or A23187 in the presence of noradrenaline or high K, but not the endothelium-dependent relaxations. In E(−) preparations, ACh (0.1–10 μM) neither increased the amount of 6-keto PGF1α nor produced a contraction. In dispersed single endothelial cells, A23187 markedly increased but 118 mM K did not modify the amount of 6-keto PGF1α. Both noradrenaline and high K increased the production of 6-keto PGF1α in the E(−) preparations but to a lesser extent than that in the E(+) preparations. This action was attenuated by indomethacin. The amplitude of the noradrenaline-and K-induced contractions was enhanced with indomethacin pretreatment in both E(+) and E(−) tissues. PGI2-Na (10 nM), reduced the amplitude of noradrenaline-induced contractions, concentration dependently and to the same extent in both E(+) and E(−) preparations. These results indicate that synthesis of PGI2 in the endothelium is not causally related to the endothelium dependent relaxation. PGI2 synthesized in the endothelium may not act directly on the muscle tissue, but PGI2 synthesized in the smooth muscle tissue may produce an inhibition of contraction.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Ca2+ channel ; smooth muscle cell ; D600 ; Ca2+ antagonist ; Ca2+ current ; intracellular perfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The voltage dependent Ca2+ inward current in single smooth muscle cells dispersed from the longitudinal muscle layer of the rabbit ileum and rabbit portal vein was recorded using the whole-cell voltage clamp technique. D600 added to the bathing solution inhibited the Ca2+ current, while the intracellular perfusion of this agent did not reduce the amplitude of this current. Thus, D600 probably acts from the outer surface of the membrane. The nature of the Ca2+ channel in smooth muscle cells seems to differ from that in cardiac muscle cells.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2013
    Keywords: Calcium ion ; Ca2+-dependent K+ channel ; Single ion channel ; Vascular smooth muscle ; Tetraethylammonium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We found a new type of Ca2+-dependent K+ channel in smooth muscle cell membranes of single cells of the rabbit portal vein. A slope conductance of the current was 180 pS when 142 mM K+ solution was exposed to both sides of the membrane (this channel was named the KM channel, in comparison to the known KL and KS channels from the same membrane patch; Inoue et al. 1985). This KM channel was less sensitive to the cytoplasmic Ca2+ concentration, [Ca2+]i, but was sensitive to the extracellular Ca2+, [Ca2+]o, e.g. in the outside-out membrane patch, lowering the [Ca2+]o in the bath markedly reduced the open probability of this channel, and also in cell-attached configuration, lowering of the [Ca2+]o using the internally perfused patch clamp electrode device reduced the opening of KM channel. TEA+ (1–10 mM) reduced the amplitude of the elementary current through the KM channel applied from each side of the membrane, but this agent inhibited the KM channel to a greater extent when applied to the inner than to the outer surface of the membrane. Furthermore, this KM channel had a weak voltage dependency, and the open probability of the channel remained much the same within a wide range of potential (from −60 mV to +60 mV). Whereas most Ca2+-dependent K+ channels are regulated mainly by [Ca2+]i and possess a voltage dependency, these properties of the KM channel differed from other Ca2+-dependent K+ channels. The elucidation of this KM channel should facilitate explanations of the actions of external Ca2+ or TEA+ on the membrane potential, in the smooth muscles of the rabbit portal vein.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1420-9071
    Keywords: Vascular smooth muscles ; Ca-induced Ca release ; skinned muscles ; pharmaco-mechanical coupling ; voltage dependent Ca-influx
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary This article was concerned with the role of Ca in triggering the contraction in vascular smooth muscles. Whenever Ca influx is activated, this Ca does not directly activate the contractile proteins, but rather triggers the release of Ca from the SR to activate calmodulin. This release of Ca by Ca is dependent on the amount of Ca stored within the cells. Voltage dependent Ca influx activated by excess concentrations of K, electrical depolarization and Ca spikes is required to produce the contraction through activation of the Ca-induced Ca release mechanism. The elucidation of the contribution of the P-I response for Ca mobilization through activation of receptors under physiological conditions hopefully will lend support to our hypothesis.
    Type of Medium: Electronic Resource
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