Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 112, Issue 5
Displaying 1-5 of 5 articles from this issue
  • Yasuharu AKI, Youichi ABE, Toshiaki TAMAKI
    1998 Volume 112 Issue 5 Pages 287-297
    Published: 1998
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    There has been an intense interest in multiple interacting paracrine systems that influence renal hemodynamics. The contractile responses at different sites along the renal vascular network exhibit distinct characteristics, depending on their receptor populations or activation mechanisms. These differences in effector mechanisms have also coupled with variations in paracrine signals from adjoining endothelial and epithelial cells. In this review, we have focused on the roles of nitric oxide (NO) and adenosine in the regulation of renal microvasculature and how they interact with other vasoactive factors. Vasopressin (VP) V2 receptors as well as V1 receptors exist in renal vasculature, especially in afferent arterioles, and V2-receptor stimulation induced vasodilation. V2-receptor-mediated vasodilation was attenuated by L-NNA. In addition, Ang II did not affect the diameter of isolated rabbit afferent arterioles, but after the treatment of L-NNA, Ang II exerted a dose-dependent vasoconstriction. Thus, NO modulated the renal vascular actions of VP and Ang II. Adenosine causes vasoconstriction via the A1 receptors, which are restricted primarily to the afferent arterioles. This selective action of adenosine suggests that adenosine exerts selective control of the renal vasculature. Adenosine augmented renal vasoconstriction by NE and Ang II via the adenosine A1 receptor, and the A1 receptor antagonist significantly reduced NE- or Ang II-induced renal vasoconstriction. The plurality of these interactions indicates that while it is very important to understand the specific direct cellular actions of each individual factor, it is equally important to understand how the various interactions are orchestrated under in vivo conditions.
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  • Mahito NAKANISHI, Hiroyuki MIZUGUCHI
    1998 Volume 112 Issue 5 Pages 299-305
    Published: 1998
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    We describe a method to prepare unilamellar fusogenic liposomes (FL) that can deliver their content directly into tissue cells and cancer cells of living animals as well as into cultured animal cells. The method consists of three important steps: 1) preparation of unilamellar liposomes encapsulating the molecules to be delivered: 2) preparation of the Sendai virus using fertilized chicken eggs; and 3) preparation of FLs by fusing UV-inactivated Sendai virus particles and naked liposomes. Purified FLs are stable at 4°C for 3 weeks and can be stored indefinitely below −70°C without loss of activity. The FL-mediated delivery is applicable to cells originating from various tissues, including those of humans, monkeys, cows, dogs, mice, rats, hamsters, and rabbits. However, human primary T cells primary B cells, and B cell lines are not susceptible to delivery. FLs are best suited to an examination of the biological activity of cytokines in the tissue cells of living animals. We also describe the possibility of developing FL-based hybrid vectors, which would mimic the functions of viruses and chromosomes.
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  • Yasuo ENDO
    1998 Volume 112 Issue 5 Pages 307-314
    Published: 1998
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The histamine-forming enzyme histidine decarboxylase (HDC) is induced in various tissues of mice in response to various physiological or inflammatory stimuli including stress, physical exercise, proinflammatory cytokines and hematopoietic cytokines. The induction of HDC also occurs in mast cell-deficient mice. The newly formed histamine produced through the induction of HDC diffuses away from its site of formation without being stored. Therefore, in addition to the release of histmine from mast cells or basophils, the induction of HDC is an important alternative mechanism for supplying histamine. Studies on the newly formed histamine may clarify new physiological or pathological roles of histamine. Here, we introduce a method that we devised for the simultaneous assay of HDC activity of many samples taken from mice. This method is based on (i) a simple method for the preparation of histamine-free enzyme solutions and (ii) a simple manual method for the separation of histamine formed in reaction mixtures containing HDC.
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  • Masako UCHII, Miyuki TAKASHIMA, Tomomi SUGIYAMA, Nobuo KOSAKA
    1998 Volume 112 Issue 5 Pages 315-321
    Published: 1998
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The effects of 3-[bis(4-hydroxyphenyl)methyl]-2-[4-(2-chlorophenyl)-piperazin-1-ylcarbonyl]-1-(2-dimethylamino ethyl) indole methanesulfonate (KW-8232) on the bone turnover in ovariectomized (OVX) rats were studied by the oral administration for 6 weeks. KW-8232 inhibited the decreased bone mineral densities of the femur and tibia in OVX rats. OVX induced the increase of serum alkaline phosphatase and osteocalcin levels, markers of high bone turnover, and also increased urinary hydroxyproline, pyridinoline and deoxypyridinoline excretion, markers of bone resorption. KW-8232 significantly inhibited the increase of serum alkaline phosphatase level at doses of 10 and 30 mg/kg and the increase of osteocalcin level at a dose of 3 mg/kg. KW-8232 (1 mg/kg) markedly suppressed the OVX-induced increase of urinary hydroxyproline, pyridinolline and deoxypyridinoline excretion. KW-8232 didn't affect serum calcium level, but significantly decreased urinary calcium excretion at doses of 10 and 30 mg/kg. These results suggest that KW-8232 decreased bone loss in this model by suppressing bone resorption.
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  • Yoshinori KATOH, Mamoru TANAKA, Hidetoshi KAWASHIMA
    1998 Volume 112 Issue 5 Pages 323-331
    Published: 1998
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    To evaluate the effects of teprenone on acute gastritis, its inhibitory effects on gastric mucosal damage were compared to that of gefarnate in taurocholate/hydrochloric acid-induced acute gastric mucosal lesions in rats. After oral administration of 160 mM taurocholic acid and 250 mM hydrochloric acid, hemorrhage and erosion were macroscopically observed in the gastric mucosal surface layer. Edema in the submucosal tissue and decreased PAS staining in the mucosa were histomorphologically observed. Concerning macroscopic findings, pretreatment with teprenone at a dose of 50 mg/kg or more significantly reduced pathological changes in the mucosa of the fundic glandular area. However, gefarnate slightly inhibited these changes in at a dose of 50 mg/kg and significantly inhibited them at a dose of 200 mg/kg. With regards to histomorphological findings in the fundic glandular area, teprenone slightly inhibited erosion at a dose of 50 mg/kg, and it significantly and slightly inhibited the decrease in PAS staining in this area at doses of 50 and 200 mg/kg, respectively. Gefarnate at doses of 50 and 200 mg/kg showed significant inhibition of decreased PAS staining in the fundic glandular area. In the pyloric mucosa, decreased PAS staining was slightly inhibited by teprenone at both doses but not by gefarnate at either dose. The differences between teprenone and gefarnate observed in this model appear to be due to their differences in mucus production ability. These results suggest that teprenone was more effective than gefarnate for the treatment of gastritis.
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