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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
    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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 319 (1982), S. 115-120 
    ISSN: 1432-1912
    Keywords: Guinea-pig small intestine ; Non-Cholinergic ; Non-Adrenergic transmission ; Role of Ca2+ ; Indomethacin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of calcium channel blockers (D-600, verapamil), sodium nitroprusside, papaverine, indomethacin, local anaesthetics and blockade of sodium pump activity on the non-cholinergic, non-adrenergic transmission in the guinea-pig duodenum, jejunum, proximal and terminal ileum were analysed in the presence of atropine and guanethidine. A decrease of the extracellular Ca2+ concentration inhibited the primary and rebound contractions but only in Ca2+-free solution was the primary relaxation diminished. D-600, verapamil, sodium nitroprusside and papaverine inhibited both the primary and rebound contractions to the same degree and their effects on the primary relaxation were less pronounced than on the contractions. Indomethacin dissolved in alkaline solution did not depress the non-cholinergic, non-adrenergic responses in any region of the small intestine, whereas indomethacin dissolved in ethanol antagonized both the primary and rebound contractions in the muscles. Local anaesthetics (procaine, trimecaine) in low concentrations inhibited only the primary contraction. Higher concentrations also inhibited both the rebound contraction and primary relaxation. Procaine in low concentrations did not markedly affect the non-cholinergic, non-adrenergic i.j.p.s and e.j.p.s., but did block the action potentials induced by e.j.p.s. Our findings indicate that the primary relaxation, and primary and rebound contractions are probably induced by different mechanisms and are not mediated by ATP. We confirmed that prostaglandins did not participate in the generation of the rebound contraction.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 319 (1982), S. 108-114 
    ISSN: 1432-1912
    Keywords: Guinea-pig small intestine ; Non-cholinergic, non-adrenergic transmission ; ATP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-cholinergic, non-adrenergic responses to nerve stimulation recorded from smooth muscles of the guinea-pig duodenum, jejunum, proximal and terminal ileum were investigated in an attempt to characterize these responses. In the presence of atropine (1–2 μmol · l−1) and guanethidine (10 μmol · l−1) coaxial stimulation induced in all regions of the guinea-pig small intestine an initial relaxation (primary relaxation) upon which contraction (primary contraction) appeared, followed by rebound contraction. Noradrenaline decreased the cholinergic smooth muscle twitches, predominantly at low stimulation frequencies, and had a similar effect on the non-cholinergic, non-adrenergic primary relaxation, primary and rebound contractions. ATP decreased the smooth muscle twitches; however, this agent had only a transient influence on the non-cholinergic, non-adrenergic responses of muscle (tension and membrane potential) to single stimuli. With higher stimulus frequencies ATP increased the primary relaxation and decreased the contraction phases. ATP also inhibited the post-tetanic inhibition induced by non-cholinergic, non-adrenergic nerve stimulation. In most of the muscle cells of the guinea-pig proximal and terminal ileum the non-cholinergic, non-adrenergic nerve stimulation generated i.j.p.s., while about 15–20% of the cells responded with e.j.p.s. During long-lasting stimulation (10s) the i.j.p.s. were sometimes “interrupted” by action potentials or by a gradual depolarization of the membrane. The i.j.p.s. were followed by a marked rebound depolarization accompanying the action potentials. Those cells which generated i.j.p.s. in response to field stimulation, were depolarized by ATP, while those cells, which generated e.j.p.s, were hyperpolarized by ATP. A reduction in the concentration of extracellular sodium chloride decreased both the primary and rebound contractions; the primary contraction was, however, more sensitive than was the rebound contraction. Theophylline increased the primary and rebound contractions with no marked influence on the primary relaxation, lowered the action potential threshold, increased the rebound depolarization and did not markedly influence the i.j.p.s. Quinidine enhanced the primary relaxation and inhibited the primary contraction in a concentration-dependent manner. Inhibition of the rebound contraction by quinidine was slight (less than 50%). The present results demonstrate that primary relaxation, primary and rebound contractions are associated with i.j.p.s and e.j.p.s., and rebound depolarization with action potentials, respectively; they are typical responses of various regions of the guinea-pig small intestine to activation of inhibitory and excitatory non-cholinergic, non-adrenergic nerves. The P1 and P2 receptors, proposed by Burnstock (1975), probably do not mediate the non-cholinergic, non-adrenergic postsynaptic responses of the guinea-pig small intestine. A possible physiological function of ATP as a mediator of non-cholinergic, non-adrenergic nerves of the guinea-pig small intestine is discussed.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1912
    Keywords: Coronary vascular smooth muscle ; Smooth muscle membrane ; Phthalazinol ; Vas deferens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In smooth muscle cells of the porcine coronary artery, phthalazinol (≦10−5 M) did not modify the membrane potential and the membrane resistance. At a concentration of 10−4 M or higher, it hyperpolarized the membrane, reduced the membrane resistance and enhanced the rectifying property of the membrane. At the concentration of 10−5 M, phthalazinol raised the threshold for the induction of a contraction and suppressed nonselectively the amplitude of the contraction evoked by application of high [K]0, acetylcholine or electrical depolarization of the membrane. Phthalazinol (10−5–10−4 M) did not modify the membrane properties of smooth muscle cells from the guinea-pig vas deferens. However, it suppressed the amplitude of the excitatory junction potentials and the facilitation phenomenon produced by repetitive stimulation at various rates. The action potential recorded from the adrenergic nerves was not affected in the presence of phthalazinol (10−5 and 10−4 M). The mean amplitude of the miniature excitatory junction potentials (m.e.j.p.s.) was not affected by treatment with phthalazinol (10−5–10−4 M), but the rate of which of m.e.j.p.s. appeared was reduced by phthalazinol (〉5×10−5 M). These results indicate that the vasodilator property of phthalazinol may result from a suppression of Ca-mobilization in both the smooth muscle cells and the adrenergic nerve terminals. The former affects the mechanical response directly and the latter leads to an inhibition of noradrenaline release.
    Type of Medium: Electronic Resource
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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 426 (1994), S. 239-246 
    ISSN: 1432-2013
    Keywords: Single smooth muscle cells ; Rabbit portal vein ; Whole-cell voltage clamp ; Voltage-dependent L-type Ca2+ current ; Inactivation ; Onset of inactivation ; Recovery from inactivation ; Window current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract With 10 mM Ba2+ as the charge carrier, inactivation of Ca2+ channel currents could be subdivided into at least two exponentials in smooth muscle cells dispersed from the rabbit portal vein by use of the wholecell configuration of the patch-clamp technique: fast and slow inactivation. All characteristics of inactivation were independent of the size of the currents. Step changes in the holding potential unveiled an extremely slow recovery and an onset of inactivation of the order of several minutes. Steady-state inactivation critically depended on the duration of the pre-steps. Inactivation curves obtained under steady-state conditions showed as shift by approximately 25 mV towards negative potentials by comparison with curves obtained using 1-s pre-pulses. This shift greatly reduced the window current. Recovery from inactivation studied with double-pulse protocols could be classified into at least two exponentials. The contribution of the slow recovery was accentuated at negative holding potentials. Recovery from inactivation critically depended on the duration of the conditioning voltage step, and was also dependent on the duration of the pre-step: its voltage dependence disappeared when pre-pulses longer than 2 s were applied. Onset of inactivation was composed of at least two exponentials: the fast component was accelerated at less negative pre-step potentials. We propose that several inactivated states are involved in Ca2+ channel inactivation. Transitions between these states are voltage dependent and voltage independent.
    Type of Medium: Electronic Resource
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  • 9
    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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  • 10
    ISSN: 1572-9540
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract μ+SR experiments were performed on delafossite-type compounds, CuCrO2, AgCrO2, CuFeO2, which are model compounds of triangular lattice antiferromagnets. The initial asymmetries are much smaller than the expected value, implying muonium formation. The time spectra are composed of slow andfast relaxation components. We attributed the components to signals from μ+ stopped at the center of O2− ions andmuonium far from nuclear dipole moments, respectively. The asymmetries decrease belowT N but no precession spectra were observed. Relaxation rates of slow andfast relaxation components show maxima atT N.
    Type of Medium: Electronic Resource
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