Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 90, Issue 1
Displaying 1-7 of 7 articles from this issue
  • Yukiyoshi YANAGIHARA, Akihide KODA
    1987 Volume 90 Issue 1 Pages 1-11
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Soluble factors released by both T and B cells are involved in the class-specific regulation of IgE antibody formation; some factors have affinity for IgE, whereas others do not. The induction phase of the primary and secondary IgE antibody response is highly sensitive to treatment with such factors or some drugs. In contrast, persistent IgE antibody formation is mostly insensitive to the same treatments, indicating that this phase differs apparently from the induction phase. Thus, it is very important to note the marked differences between the regulatory mechanisms of these two phases when drugs responsible for the suppression of IgE antibody response are developed. In the present review, the recent advances pertaining to the regulation of IgE antibody formation in animals and humans are described in view of immunopharmacology.
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  • (3) Studies on the vasodilating effects in isolated monkey arteries and the peripheral hypotensive mechanism in SHR
    Shigeyuki NAKAJIMA, Motohiko UEDA
    1987 Volume 90 Issue 1 Pages 13-21
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Vasodilating effects of pinacidil in isolated monkey arteries were compared with those of nifedipine and hydralazine, and the relationship of the central nervous system to hypotensive and positive chronotropic effects of pinacidil in SHR was also studied. In arterial strips contracted with prostaglandin F, the relaxant potencies of pinacidil were in the order of mesenteric=femoral>basilar=middle cerebral arteries, whereas those of nifedipine were middle cerebral=basilar=coronary>femoral arteries, and those of hydralazine were femoral>middle cerebral=coronary arteries. In pithed SHR, the hypotensive effect of pinacidil was dose-related, similar to hydralazine. Intravenous administration of 0.1 and 0.3 mg/kg of pinacidil in SHR demonstrated remarkable hypotension, whereas intracerebroventricular administration of the same doses did not show any significant effects. Therefore, the central autonomic nervous systems did not seem to take part in the hypotensive effects of pinacidil. The hypotension by intravenous administration of pinacidil in SHR was followed by an increase in heart rate. The increase in heart rate in conscious SHR was more marked than that in anaesthetized SHR. In pithed SHR, pinacidil did not show positive chronotropic effects even with the larger dose of 3 mg/kg, i.v. Propranolol pretreatment inhibited the increase in heart rate produced by pinacidil. These results show that the increase in heart rate following hypotension produced by pinacidil were caused by the activation of efferent sympathetic nerves via the baroreceptor. The peripheral hypotensive mechanism of pinacidil was supported by the present results.
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  • Toshio OBATA, Toru EGASHIRA, Yasumitsu YAMANAKA
    1987 Volume 90 Issue 1 Pages 23-31
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Monkey liver monoamine oxidase (MAO) was predominantly the B-form enzyme from the observed differences in substrate specificities and differences in sensitivities to MAO inhibitors. It is known that a MAO inhibitor, pargyline, binds to MAO irreversibly in the molar ratio of 1: 1. 3H-pargyline was used as a marker to determine the existance of MAO. The molecular weight of MAO in monkey liver mitochondria was investigated by SDS-polyacrylamide gel electrophoresis after solubilization of 3H-pargyline binding mitochondria with 6% sodium dodecyl sulphate (SDS). The subunit molecular weight was found to be 60, 000. The molecular weight determined from the electrophoretic mobility on several concentrations of gels by disc gel electrophoresis in the absence of SDS was found to be 120, 000. These results indicate that monkey liver mitochondrial MAO exists as a dimer. Isoelectric focusing of the enzyme after solubilization with 0.1% Triton X-100 and 0.75% Triton X-100 and 0.75% Lubrol showed that it had a pI value near 6.5. Similar pI values were obtained for enzyme preparations solubilized with 0.75% Triton X-100 after treatment with phospholipase A or methylethylketone. These results suggest that the pI value of MAO in monkey liver mitochondria does not depend on the properties of detergents used to solubilize the enzyme preparation.
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  • Michio ABE, Yasuhiko ONO, Yoshinobu YAMAZAKI, Arao UJIIE, Shigeru IKED ...
    1987 Volume 90 Issue 1 Pages 33-40
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Effect of terodiline on isolated rabbit and guinea pig detrusor was investigated in comparison with that of flavoxate and oxybutynin. Terodiline (10-6M) parallelly shifted the dose-response curve for carbachol in rabbit detrusor to the right, and high doses of terodiline (3×10-6 ?? 3×10-5 M) inhibited the maximal contraction. Flavoxate (10-5 M or more) also inhibited the maximal contraction. Oxybutynin (10-8 M or more) shifted the dose-response curve to the right, but did not affect the maximal contraction. At 3 × 10-6 M or more, terodiline dose-dependently inhibited the Ca-contraction of rabbit detrusor. While the contraction of rabbit detrusor induced by electrical field stimulation was inhibited by atropine (3 × 10-7 M) or nifedipine (3 × 10-6 M) by 35% or 73%, respectively, the combination of atropine (10-7 M) and nifedipine (10-6 M) abolished it. Oxybutynin (3 × 10-7 M) inhibited it by about 30%; terodiline (10-6 M or more) and flavoxate (10-5 M or more) dose-dependently inhibited it, and abolished at 10-4 M and 3 × 10-4 M, respectively. Terodiline inhibited the 1-quinuclidinyl-[phenyl-4-3H]-benzilate binding to the microsomal fraction of guinea pig urinary bladder, brain, atria and ileum dose-dependently, and it had similar affinity among these fractions. Terodiline (3 × 10-6 M or more) inhibited the 45Ca uptake to minced guinea pig urinary bladder dose-dependently, but did not influence the 45Ca efflux even at 10-4 M. Flavoxate (10-4 M) only slightly inhibited the 45Ca uptake. The present result suggests that the inhibitory action of terodiline on the contraction of detrusor is attributable to the anti-muscarinic and Ca-antagonistic effect, and terodiline has a different pharmacological property from oxybutynin and flavoxate.
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  • The effect on monoamine uptake and turnover in mouse brain
    Michihide SETOGUCHI, Shuzo TAKEHARA, Masamitsu SAKAMORI, Koretake ANAM ...
    1987 Volume 90 Issue 1 Pages 41-49
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    The effect of Y-8894 (±) 2-[[o-(2-thenyl)phenoxy]methyl] morpholine maleate, which has been shown to improve experimentally induced learning and memory deficits, on cerebral monoamine uptake and turnover was studied in the mouse. The following results were obtained: 1) It inhibited in vitro norepinephrine (NE) uptake to the mouse cerebral synaptosomal fractions about 800 and 1250 times more potently than it did those of dopamine (DA) and serotonin (5-HT), respectively. 2) It dose-dependently inhibited in vivo NE uptake, but not DA or 5-HT uptake. 3) It reduced the accumulation of the NE metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), increased that of the 5-HT metabolite, 5-hydroxyindoleacetic acid (5-HIAA), and had no effect on that of the DA metabolite, homovanillic acid (HVA). These effects were compared with those of imipramine, calcium hopantenate (Ca-hopantenate) and dihydroergotoxine. Y-8894 appeared to act by stimulating the noradrenergic receptor, and it acts to a lesser extent by blocking the serotonergic receptor in the brain.
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  • Shigefumi TAKEDA, Yoshio KASE, Ichiro ARAI, Yasufumi OHKURA, Masayuki ...
    1987 Volume 90 Issue 1 Pages 51-65
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    TJN-101 ((+)-(6S, 7S, R-biar)-5, 6, 7, 8-tetrahydro-1, 2, 3, 12-tetramethoxy-6, 7-dimethyl-10, 11-methylenedioxy-6-dibenzo[a, c]cyclooctenol) is one of the lignan compounds isolated from Schisandra fruits. 1) Effect of TJN-101 on liver fibrosis was investigated in rats which were injected with CCl4 (1 ml/kg) subcutaneously twice a week for 12 weeks. TJN-101 was given orally at the dose of 10 or 30 mg/kg/day for 6 or 3 weeks beginning on the 6th or 9th week after the start of CCl4-intoxication, respectively. The elevations of serum transaminase activities and the increase of liver 4-hydroxyproline content were observed depending on the period of CCl4-intoxication. These changes were marked on the 9th and 12th weeks after. In the histopathological study, the degenerative fatty change on the 6th week after and the formation of pseudolobule caused by fibrosis proliferation on the 9th or 12th week after were mainly observed. When rats were treated with TJN-101, the abnormalities in biochemical parameters and the fibrosis proliferation caused by CCl4-intoxication were improved. 2) Chronic liver injury was induced by the treatment with CCl4 (1 ml/kg) subcutaneously twice a week for 10 weeks to investigate the effect of TJN-101 on liver regeneration after partial hepatectomy. TJN-101, which was given orally at the dose of 10, 30 or 100 mg/kg/day for 6 days from the 1st day after partial hepatectomy, dose-dependently increased the liver regeneration rate and improved the serum BSP retention rate. These results suggest that TJN-101 suppresses the fibrosis proliferation and accelerates both the liver regeneration and the recovery of liver function after partial hepatectomy in chronic liver injury.
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  • Effect of Neurotropin on immunosuppression caused by stress
    Takao MATSUOKA, Haruo YOSHII, Seishi SUEHIRO
    1987 Volume 90 Issue 1 Pages 67-71
    Published: 1987
    Released on J-STAGE: February 23, 2007
    JOURNAL FREE ACCESS
    Neurotropin is an extract isolated from the inflamed skins of rabbits inoculated with Vaccinia virus. A study was carried out to examine the effect of Neurotropin on the immunosuppressions caused by stress. Mice were restrained for 16 hr per day for 2 consecutive days. Under this condition, the immune responses such as PFC and DTH to SRBC, T cell-dependent antigen, were markedly suppressed. Moreover, the phagocytic activity of macrophages were also suppressed. Neurotropin was found to restore such suppressions of both T cell response and phagocytosis in stressed mice. These results suggest that the effect of Neurotropin on depressed immunity in stressed mice were not only restoration of T cell function but also phagocytic activity of macrophages. Neurotropin had no effect on intact immune responses without stress. This suggests that Neurotropin can he used as an effective immunomodulator.
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