Journal of Smooth Muscle Research
Online ISSN : 1884-8796
Print ISSN : 0916-8737
ISSN-L : 0916-8737
Volume 32, Issue 5
Displaying 1-5 of 5 articles from this issue
  • Ryo SUZUKI
    1996 Volume 32 Issue 5 Pages 175-194
    Published: 1996
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
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  • WITH SPECIAL REFERENCE TO ITS ACTION IN THEPRESENCE OF PLATELETS
    Tsutomu MICHIBAYASHI
    1996 Volume 32 Issue 5 Pages 195-202
    Published: 1996
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    There have not been as many studies of vascular responsiveness to the platelet activating factor (PAF) as one might expect. The mechanism of PAF's action on blood vessel contractility has not yet been elucidated. In this study, using the isolated perfused arterial segment of the central artery of a rabbit ear and autologous platelets, we examined the effects of PAF on the vasocontractile response to noradrenaline (NA-R).
    We obtained the following results: (1) In the absence of platelets, i.e., under the conditions of perfusion with modified normal Krebs' solution alone, PAF (0.036 to 33ng/ml) had no significant influence on NA-R and basal perfusion pressure (BPP); (2) during infusion of platelet rich plasma (PRP) with PAF, NA-R was significantly more augmented, as compared with that during infusion of PRP without PAF; (3) there was no significant difference between BPP during infusion of PRP alone and that during infusion of PRP with PAF; and (4) during infusion of PRP with PAF, NA-R was alleviated by the application of ketanserin, a selective 5-HT2 receptor antagonist, while this response was little influenced by indomethacin, a cyclo-oxygenase inhibitor.
    On the basis of these results, it is possible to conclude that PAF acts on blood vessel contractility through platelets, and that 5-HT may, at least in part, participate in augmenting NA-R by PRP with PAF rather than prostanoids.
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  • Satoru TAKEKAWA
    1996 Volume 32 Issue 5 Pages 203-212
    Published: 1996
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    Colonic motility curve was continuously recorded in dog using a strain gauge force transducer and the curve was analyzed by fast Fourier transform.
    (1) The basic pattern of the colonic motility curve was a gradually increasing and decreasing contractile wave.
    (2) The frequency components of the basic contractile wave showed a trimodal distribution with peaks at around 1, 20 and 80mHz.
    (3) The 1mHz component showed a sine curve and represented the slow, big motion in the basic contractile wave.
    (4) The 20mHz component represented the relatively rapid, gradually increasing and decreasing, big motion in the basic contractile wave.
    (5) The 80mHz component represented the rapid, small motion in the basic contractile wave.
    (6) The fundamental frequency components of the colonic contractile wave were unchanged before and after defecation.
    (7) For the antiperistaltic wave which disappeared during transmission, the peaks of the wavelength components weakened during transmission and the wave progressed to a multi-modal curve.
    Our findings indicate that fast Fourier transform is an extremely useful method in elucidating colonic motility.
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  • Ryo SUZUKI
    1996 Volume 32 Issue 5 Pages 213-218
    Published: 1996
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    The function and sites of action of prostaglandins (PGs) vary in different animal species and tissues. In this study the effects of PGs (E1, E2, F2α, D2) on intraocular muscles and outflow facility of the eye were investigated, using enucleated bovine eyes. None of these PGs exogenously applied influenced the neuromuscular transmission. By contrast, after treatment with indomethacin, all PGs tested contracted the muscle much more than in the absence of indomethacin, and under these conditions the PGs potentiated responses to cholinergic nerve stimulation. Whereas PGF was less potent in the absence of indomethacin, PGF2α had more potent action primarily on nerves and partly on muscles after treatment with indomethacin. PGs also increased outflow facility of the eye, after the treatment with indomethacin. In order to understand the site and action of PGs, pretreatment with indomethacin may be useful in the intraocular muscle and outflow facility of the eye.
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  • Kazumasa SHIMIZU, Tamami ABE, Shinjiro NAKAJYO, Norimoto URAKAWA, Miki ...
    1996 Volume 32 Issue 5 Pages 219-228
    Published: 1996
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    Two substances identified as ((3β, 4α, 16β, 21β, 22α)-21-tigloxy-16, 22, 23, 28-tetrahydroxyolean-12-en-3-yl-β-D-glucopyranosiduronic acid) (GA1) and ((3β, 4α, 16β, 21β, 22α)-21-(2-methylbutyroxy)-16, 22, 23, 28-tetrahydroxyolean-12-en-3-yl-β-D-glucopyranosiduronic acid) (GA2) identified among the gymnemic acids are triterpene glycosides extracted from Gymnema sylvestre leaves. We examined the effects of GA1 or GA2 on high K+-induced contraction in the guinea-pig longitudinal muscle. A sustained muscle contraction induced by hyperosmotically added 65.4mM KCl (H-65K+) was suppressed by GA1 or GA2 (7.7×10-5M). Simultaneous measurements of reduced pyridine nucleotide (PNred) or oxidized flavin protein (FPox) by the fluorescence technique and of contractile force revealed that GA1 and GA2 reduced the increase of PNred fluorescence and contractile force induced by H-65K+, whereas FPox fluorescence induced by it further increased. Reduced muscle contraction induced by GA1 or GA2 was restored by 5.5mM pyruvate. Simultaneous measurements of intracellular Ca2+ [Ca2+] i level and contractile force indicated that [Ca2+] i level, which increased by H-65K+, hardly changed with GA1 and GA2. In summary, both GA1 and GA2, which are among the gymnemic acids, suppressed high K+-induced contraction in the guinea-pig ileal longitudinal muscle. The difference between these two gymnemic acids was not significant. The inhibitory effect of GA1 and GA2 on smooth muscle were assumed to be a result of inhibiting glucose uptake, which is an energy source of the muscle, whereas the inhibitory mechanisms were probably not mediated by Ca2+.
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