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Volume 109, Issue 1
Displaying 1-5 of 5 articles from this issue
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Takafumi NAGATOMO, Yoshiaki HOSOHATA, Toshio OHNUKI, Jun SUZUKI1997 Volume 109 Issue 1 Pages 1-12
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSThe non-selective β-blocker bopindolol, which was developed as a pro-drug, possessed 50-60 times more potent long-acting hypotensive effects on the blood pressure than those of atenolol or propranolol. Because this drug has only a mild partial agonist activity, it did not cause the rapid decrease in heart rate observed with atenolol or propranolol or the increase in heart rate induced by pindolol. These hypotensive effects are due to β1-antagonistic effects, not effects on β2- orβ3-adrenoceptors. In addition to these effects, benefits of this drug include the following: slow dissociation rate from β-adrenoceptors in tissues, high affinity to 5-HT1A subtypes, less clinical effects on lipid metabolism and the inhibition of renin release. It is possible that this drug possesses different pharmacological characteristics from other β-blockers.View full abstractDownload PDF (9911K) -
Yuji SAITO1997 Volume 109 Issue 1 Pages 13-17
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSrho p21 is a member of the ras superfamily of small GTPases. Clostridium botulinum C3 exoenzyme ADP-ribosylates rho p21 at the Asp41 residue located at an effector domain and inhibits its biological activity by interfering with the interaction with its downstream effectors. The amount of rho p21 in cells or tissues is determined by the in vitro ADP-ribosylation reaction with C3 exoenzyme and 32P NAD. The studies using C3 exoenzyme have revealed that rho p21 is involved in the regulation of stress fiber formation, cell adhesion, contractile ring formation during cytokinesis and serum response factor-mediated activation of immediate early genes. C3 exoenzyme is a valuable tool for elucidating the unidentified function of rho p21 because the exoenzyme specifically inhibits rho p21-mediated signal transduction pathways. A Glu173-substitution mutant of the C3 exoenzyme lacking ADP-ribosyltransferase activity is useful for a control experiment.View full abstractDownload PDF (4520K) -
Yasushi HIGASHIDE, Yoriko YATABE, Yoko ARAI, Masahiro SHIBATA, Tetsuak ...1997 Volume 109 Issue 1 Pages 19-29
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSWe examined the effect of a novel tachykinin NK-2-receptor antagonist, Nα-(tert-Butylcarbamoyl)-L-glutaminyl-L-tryptophyl-α-aza-phenylalanine 2-benzyloxyethylamide (TAC-363), on hyperventilation- and citric acid-induced bronchoconstriction and neurokinin A (NKA)-, capsaicin- and antigen-induced airway hyperresponsiveness in guinea pigs. The i.v. administration of TAC-363 at doses of 0.01-1 mg/kg inhibited hyperventilation- and citric acid-induced bronchoconstriction in a dose-dependent manner, while FK-888, a tachykinin NK-1-receptor antagonist, did not inhibit hyperventilation-induced bronchoconstriction. NKA-induced airway hyperresponsiveness to acetylcholine was attenuated by i.v. injection of TAC-363, but not by the thromboxane A2 synthetase inhibitor ozagrel and the mast cell stabilizer DSCG. Furthermore, TAC-363 prevented the occurrence of capsaicin- and antigen-induced airway hyperresponsiveness to acetylcholine, while FK-888 did not prevent occurrence of capsaicin-induced airway hyperresponsiveness. In summary, TAC-363 inhibits bronchoconstriction and airway hyperresponsiveness induced by various stimuli. These results suggest that NKA mediates bronchoconstriction and airway hyperresponsiveness. Thus, TAC-363 is expected to be useful in the treatment of airway diseases such as asthma.View full abstractDownload PDF (8745K) -
Sadayoshi ONODERA, Masato TANAKA, Niro INABA, Takao SUZUKI, Masahiro S ...1997 Volume 109 Issue 1 Pages 31-40
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSOral administration of an ammonia solution (0.01 %) or a sodium taurocholate solution (TCA solution, 5 mM) as drinking water for 4 weeks or 13 weeks, respectively, resulted in gastric mucosal thinning and decreased parietal cell numbers. Oral administration of TCA solution also caused cell infiltration in the lamina propria of the mucosa and mucosal fibrosis. When lafutidine (3, 10 mg/kg) was administered orally once daily for one week after the withdrawal of ammonia or TCA solution, the recovery of the mucosal thickness in the fundic gland area and the parietal cell number were significantly accelerated, and the recovery of mucosal thickness in the pyloric gland area also tended to be accelerated. Lafutidine at 10 mg/kg for 1 week had no influence on normal mucosal thickness and parietal cell numbers. At the doses that produce equal or greater acid antisecretory effect than lafutidine, oral administration of cimetidine (30 mg/kg) and famotidine (1 mg/kg) had no effect on either of these atrophy indexes. These results demonstrate that lafutidine, unlike cimetidine and famotidine, can accelerate the healing of mucosal injuries in ammonia- and TCA-induced chronic gastritis models.View full abstractDownload PDF (8027K) -
Yuji NAGAO, Haruo MIYATA, Kiyoshi MIZUGUCHI, Minako BAN, Katsuaki KATO1997 Volume 109 Issue 1 Pages 41-52
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSWe examined the effect of ulinastatin in comparison with prednisolone (PSL) and salazosulfapyridine (SASP), well-known drugs for ulcerative colitis (UC), on two experimental UC models induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNB) in rats. Ulinastatin at the doses of 3000-10000 units/kg/day (i.v.) significantly ameliorated the formation of erosion and infiltration of inflammatory cells in colonic mucosa in DSS-induced rat UC models. Moreover, ulinastatin at the dose of 10000 units/kg/day (i.v.) significantly suppressed inflammation with ulcer in the colonic mucosa in TNB-induced rat UC models. PSL at the dose of 1 mg/kg/day (p.o.) also was as effective as ulinastatin on the above two UC models, while SASP at the dose of 100 mg/kg/day (p.o.) was less effective than ulinastatin and PSL. In addition, ulinastatin inhibited the activities of elastase and cathepsin G from human leukocytes, and it suppressed TNF α, IL-8 and superoxide production by rat macrophages and rabbit leukocytes in vitro. These results suggest that the suppression of inflammatory mediators produced by leukocytes is involved in the mechanism of the anti-UC action of ulinastatin.View full abstractDownload PDF (9078K)
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