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Volume 97 (1991)
- Issue 6 Pages 307-
- Issue 5 Pages 241-
- Issue 4 Pages 179-
- Issue 3 Pages 135-
- Issue 2 Pages 51-
- Issue 1 Pages 1-
Volume 97, Issue 6
Displaying 1-7 of 7 articles from this issue
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-—For a better understanding of the mechanisms of relaxation of smooth muscleShoichi IMAI1991 Volume 97 Issue 6 Pages 307-318
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSFirst, we will briefly describe how our study on the mechanisms of relaxant effects of nitroglycerin and related compounds (NG) on the vascular smooth muscle developed to a study on the sarcolemmal (SL) Ca2+-ATPase. These compounds were found to have no effects on the voltage-dependent Ca2+ channel and Ca2+-induced Ca2+ release from the sarcoplasmic reticulum (SR) and Na+-Ca2+ exchange mechanism has been shown not to play an important role in the vascular smooth muscle. Furthermore, when we initiated our study, the idea of receptor-operated Ca2+ channels and Ca2+ release from the SR by inositol triphosphates were not known. A major part of this review is devoted to a description of the characteristic features of SL Ca2+-ATPase and its regulation by various protein kinases. References to SR enzyme are made when necessary. Brief mention is made of the putative molecular structure and its possible variations as envisaged by genetic engineering techniques. However, particular attention is directed to the regulation by cyclic GMP-dependent protein kinase as this seems to be most important as regards the mechanisms of vascular smooth muscle relaxation by NG.View full abstractDownload PDF (10472K) -
Haruo TAKEMURA, Hideyo OHSHIKA1991 Volume 97 Issue 6 Pages 319-327
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSInositol phosphates have an important role in Ca2+ mobilization and especially inositol 1, 4, 5-trisphosphate (IP3) is now believed to release Ca2+ from the endoplasmic reticulum (ER) . On the other hand, the mechanism of activation of Ca2+ entry is unknown. Non-excitable cells have only receptoroperated Ca2+ channels, lacking voltage-operated Ca2+ channels, and are a useful system for studying signal transduction. In this review, some mechanisms for the regulation of Ca2+ entry in non-excitable cells are discussed and a new hypothesis originally proposed by Putney (1986), the capacitative Ca2+ entry model, is focussed. In this model, Ca2+ influx across the plasma membrane is increased when the IP3-sensitive Ca2+ pools is emptied. Capacitative Ca2+ entry is now confirmed in rat parotid acinar cells by studies on the refilling process for intracellular Ca2+ pools and by using the microsomal Ca2+ATPase inhibitor thapsigargin, which does not increase cellular IP3. Finally, capacitative Ca2+ entry is expected to exist in a variety of cell types including excitable cells.View full abstractDownload PDF (7465K) -
Yu YAMAGUCHI, Machiko HAYASHI, Hiroshi YAMAZOE, Masaru KUNITOMO1991 Volume 97 Issue 6 Pages 329-337
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThis study examined the preventive effects of green tea extract on hyperlipidemia and lipid accumulation in the liver and aorta of mice fed an atherogenic diet enriched with 1.5 % cholesterol, 0.5 % cholic acid and 5% linoleic acid for a period of 14 weeks. The animals were given green tea extract in drinking water at doses of 50, 100 and 200 mg/kg/day. Treatment with green tea extract prevented the increase of serum cholesterol induced by the atherogenic diet 6 weeks after the start of the experiment. The increase of serum lipid peroxides was markedly prevented in a dose-related manner. The green tea extract also tended to prevent the increase of serum phospholipid and the decline of lecithin : cholesterol acyltransferase, but could not prevent decreases in serum triglycerides and high-density lipoprotein cholesterol. As for liver cholesterol, its content, particularly free cholesterol, in mice fed the atherogenic diet could be prevented from increasing by treatment with the extract at 50 and 100 mg/kg/day. In addition, the increase of aortic cholesterol, particularly esterified cholesterol, could be prevented in a dose-related manner. These results suggest that green tea has anti-atherosclerotic activity.View full abstractDownload PDF (7493K) -
Toru EGASHIRA, Takayuki NAGAI, Yoshihira KIMBA, Fumie MURAYAMA, Shinic ...1991 Volume 97 Issue 6 Pages 339-350
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSCellular damage of various organs by ischemia following reperfusion is assumed to be at least in part due to lipid peroxidation in biomembranes, and oxygen-derived free radicals play a major role. The level of lipid peroxides in liver tissue increased during 90-min ischemia. When reflow of hepatic blood was allowed, a greater increase in the lipid peroxides was observed. Similar increases were obtained in several serum markers (GOT, GPT and LDH) during the period of ischemia or ischemia-reperfusion. In addition, levels of cytochrome p-450 and NADPH cyt. c reductase activity decreased in proportion to the decrease in microsomal proteins during ischemia or ischemia-reperfusion. On the other hand, superoxide dismutase in blood was significantly increased by ischemia-reperfusion. Rats died within 2 days after liver ischemia of 90 min, while all animals subjected to 30-min ischemia survived. Histopathological examinations indicated that extensive coagulation with erythrocytes occurred and the extent was dependent on the time of ischemia. The liver injury by ischemia-reperfusion could be a useful experimental model for studying liver injury induced by free radicals, for developing hepatoprotective drugs, or for investigating liver transplantation.View full abstractDownload PDF (13705K) -
Yoshihiro HIRAGA1991 Volume 97 Issue 6 Pages 351-359
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSBehavioral impairment induced by the muscarinic anticholinergic drug, scopolamine (SCP) has been widely used to make preclinical evaluation of nootropic drugs. To further investigate the disruptive effect of SCP on memory-related behavior, male Wistar-Imamichi strain rats were tested in the 8-arm radial maze task with a delay interval between choices 4 and 5. In this task, the animals were first allowed to obtain 4 food rewards out of 8 arms and then removed from the maze. They were replaced on the maze to collect the remaining 4 pellets after a delay interval, during which they were kept in their home cages. In experiment 1, a 1-6 hr delay interval was imposed. SCP (0.5 mg/kg, i.p.) was administered immediately after choice 4. In experiment 2, a delay interval was always 4 hr, but SCP was administered 0-2 hr after choice 4. In both experiments, SCP significantly reduced the number of correct choices in choices 5-8, but did not show any effects depending on delay intervals or drug-administration time. These results suggest that the performance deficits induced by SCP might be due to its effects on the primary stage of information processing rather than those on the consolidation or storage process of memory.View full abstractDownload PDF (8326K) -
Nobuyuki NISHIDA, Yoshitaka YASUHARA, Sukehiro CHIBA1991 Volume 97 Issue 6 Pages 361-369
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSFour groups of rats were trained to discriminate between the no-drug condition (saline, s.c.) and the effect of s.c. injection of the novel enkephalin analog Tyr-D-Met(O)-Gly-EtPhe-NHNHCOCH3·AcOH (EK-399, 1 mg/kg), morphine (3 mg/kg), ethylketocyclazocine (EKC, 0.3 mg/kg) or N-allylnormetazocine (NANM, 3 mg/kg) in a two-lever choice, water reinforced procedure. All groups of animals acquired the ability to discriminate EK-399, morphine, EKC or NANM from saline. Naloxone (0.03 ?? 0.3 mg/kg, s.c.) completely antagonized the discriminative stimulus effects of EK-399, morphine and EKC, but not that of NANM. In stimulus generalization tests, morphine (10 mg/kg) and buprenorphine (0.03 mg/kg), μ-opioid receptor agonists, completely substituted for EK-399 in groups trained with EK-399, whereas EK-399 (0.1 ?? 3 mg/kg) only partially substituted for morphine in rats trained with morphine. EKC (0.01 ?? 0.1 mg/kg), a ir-opioid receptor agonist, partially substituted for EK-399, and EK-399 (0.13 mg/kg) partially substituted for EKC. NANM (0.3 ?? 10 mg/kg), a σ-receptor agonist, partially substituted for EK-399, but EK-399 (0.1 ?? 3 mg/kg) did not substitute for NANM. These results suggest that the discriminative stimulus effect of EK-399 in rats mainly involves μ-opioid receptor-mediating action and also involves, to a lesser extent, other receptor (probably δ-opioid receptor) -mediating actions.View full abstractDownload PDF (7505K) -
Sunao KAWANO, Nobuhiro SATO, Takenobu KAMADA, Katsuya YAMASAKI, Takash ...1991 Volume 97 Issue 6 Pages 371-380
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe protective effect of rebamipide against 0.15 N HCl solution containing 40%ethanol (HCl-ethanol) induced mucosal lesion in the stomach was evaluated in rats and humans. In rat experiments : (1) rebamipide prevented development of mucosal damage induced by HCl-ethanol in a dose-dependent manner when tested at 10, 30, 100 and 300 mg/kg, i.p., and the prevention at 30 ?? 300 mg/kg was significant (P < 0.05) ; (2) rebamipide significantly (P < 0.05) increased mucosal blood flow by continuous i.v. dosing at 10 mg/kg/hr by the hydrogen gas clearance method; (3)rebamipide at 10 mg/kg, i.v., also significantly (P < 0.05) inhibited reduction in gastric mucosal blood volume and tended to suppress oxygen saturation of hemoglobin following hemorrhagic shock by organ reflectance spectrophotometry. A double-blind crossover study was conducted to compare the gastric protective effect of rebamipide with an inactive placebo using 6 healthy male volunteers. Rebamipide was administered to them at a clinical dose of 300 mg/day orally for 7 days, and then HCl-ethanol was given once to induce mucosal damage. Rebamipide significantly (P < 0.05) inhibited formation of mucosal lesion, decrease in the number of mucous granules and dilatation of intercellular space. These clinical findings indicate that rebamipide was protective against HCl-ethanol-induced gastric lesion at a clinical dose, and the mechanism of this gastric effect was considered to involve, in part, the improvement of mucosal microcirculation.View full abstractDownload PDF (9452K)
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