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  • 11
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    International Journal of Biochemistry 8 (1977), S. 745-751 
    ISSN: 0020-711X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 12
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Magnetism and Magnetic Materials 104-107 (1992), S. 825-826 
    ISSN: 0304-8853
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 13
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Magnetism and Magnetic Materials 104-107 (1992), S. 859-860 
    ISSN: 0304-8853
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 14
    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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  • 15
    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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  • 16
    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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  • 17
    ISSN: 1432-2013
    Keywords: Key words Venom ; Ca2+ channel ; Dihydropyridine ; Ca antagonist ; Vascular cell ; Blood vessel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Effects of synthesized calciseptine (CaS), found naturally in the venom of the black mamba, on voltage-dependent Ca2+ channels in smooth muscle cells of the guinea-pig portal vein were investigated. In the whole-cell voltage-clamp configuration, extracellular application of CaS (≥ 10 nM) inhibited the inward current in a concentration- and voltage-dependent manner at a holding potential of –90 mV. The Ca2+ current recorded at a high holding potential (–50 mV) was approximately 8 times more sensitive to CaS than that at a more negative holding potential (–90 mV). CaS (50 nM) shifted to the left the steady-state inactivation curve obtained by using single 8-s conditioning pulses of various amplitudes. When CaS (≥ 200 nM) was present in the pipette, the Ca2+ current remained for the duration of the experiments (more than 60 min) in the whole-cell configuration. Two different Ca2+ channel conductances are present in this tissue (25-pS and 12-pS channels). Both channels are blocked by dihydropyridine (DHP) derivatives, but have different sensitivities. In the cell-attached condition, CaS hardly changed the activity of either unitary Ca2+ channel current. To prevent the ”run down” of the Ca2+ channels in cell-free conditions, we added cardiac cytosol, a supernatant from homogenized cardiac cells and an endogenous Ca2+ channel activating factor, in the pipette. The unitary Ca2+ channel currents were then recorded using the outside-out membrane patch configuration. Application of CaS (1 μM) in the bath completely blocked the open events of the 25-pS Ca2+ channel. CaS (10 nM) in the bath reduced the mean open time and channel availability, resulting in a decrease in the open probability of the 25-pS channel currents without affecting the amplitude of the single-channel conductance. CaS also reduced the open probability (though less potently) and channel availability of the 12-pS Ca2+ channel without a change in its amplitude. From these results, we conclude that CaS has inhibitory effects on the voltage-dependent Ca2+ current that are similar to those of DHP derivatives and that it acts from the outside of the membrane.
    Type of Medium: Electronic Resource
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  • 18
    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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  • 19
    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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  • 20
    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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