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Volume 43 (1987)
- Issue 4 Pages 335-
- Issue 3 Pages 247-
- Issue 2 Pages 113-
- Issue 1 Pages 1-
Volume 43, Issue 3
Displaying 1-11 of 11 articles from this issue
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Kumi SUGIHARA, Sachiko NAKANO, Michiko KODA, Katsumi TANAKA, Nobuyuki ...1987 Volume 43 Issue 3 Pages 247-252
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSCisplatin (cis-diamminedichloroplatinum II), an anticancer chemotherapeutic agent with the dose-limiting side effect of nephrotoxicity, caused a statistically significant increase in lipid peroxidation, monitored by measuring the production of malondialdehyde, in rat kidney 72 hr after injection. Treatment of rats beforehand with the antioxidant α-tocopherol or N-N'-diphenyl-p-phenylenediamine (DPPD) effectively decreased such peroxidation. DPPD was a more effective inhibitor than α-tocopherol, since it is known for its ability to scavenge free radicals more powerfully. The ability of renal cortical slices to accumulate p-aminohippurate (PAH) was examined as a biochemical parameter that would change in nephrotoxicity. The ability to accumulate PAH by the incubated slices decreased 72 hr after administration of cisplatin. The pretreatment with DPPD prevented the decrease in PAH accumulation in the slices from rats treated with cisplatin. Structural changes of the renal proximal tubule caused by cisplatin, analyzed in a transmission electron microscope, were also prevented by the pretreatment with DPPD. The results suggest that cisplatin affects renal tissues in which free radicals generated by cisplatin may interact with membrane lipids to cause the production of lipid peroxidation, which affects both cellular structure and function.View full abstractDownload PDF (474K) -
Hiroko TOGASHI, Mitsuhiro YOSHIOKA, Masaru MINAMI, Keiichi SHIMAMURA, ...1987 Volume 43 Issue 3 Pages 253-261
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn order to elucidate the role of substance P in adrenal nerve activity, the effects of substance P antagonists on 1) tonic activity of the adrenal sympathetic nerve, 2) the response to exogenous substance P and 3) cutaneo-adrenal nerve reflex were investigated in anesthetized rats. Substance P or its antagonist [(Arg1, D-Trp7, 9, Leu11 )-substance P: spantide] was injected into the subarachnoid space via polyethylene tubing. Intrathecal administration of spantide (0.1-10 μg) produced a slight and transient increase in tonic activity of the adrenal nerve. Thereafter, a marked and prolonged decrease in adrenal nerve activity was observed, along with a decrease in arterial blood pressure. Intrathecally administered substance P (0.1-10 μg) produced a marked increase in tonic activity of the adrenal nerve in a dose-related manner. This substance P-induced increase in adrenal nerve activity was significantly antagonized by pretreatment with spantide. It was also found that spantide depressed the reflex response in adrenal nerve activity evoked by noxious mechanical pinching of the skin. These findings suggest the possibility that on the spinal level, substance P has an important role in the maintenance of tonic activity of the adrenal nerve and the transmission of nociceptive information to the adrenal nerve in rats.View full abstractDownload PDF (460K) -
Satoshi YUASA, Yoshihide NAKAO, Kohei UMEZU1987 Volume 43 Issue 3 Pages 263-266
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTritoqualine (TRQ) was previously reported to suppress enzyme leakage and lipid peroxidation induced by carbon tetrachloride in isolated hepatocytes. In the present study, we investigated the effect of TRQ on enzyme leakage from rat primary-cultured hepatocytes using D-galactosamine (GaIN) which causes hepatic injury without lipid peroxidation. Leakage of GPT and GPT was significantly increased at 18 hr after GaIN addition, being saturated at 42-50 hr. This enzyme leakage was suppressed dose-dependently by TRQ at 42 hr, but not by vitamin E. These results suggest that TRQ shows a suppressive effect on enzyme leakage from hepatocytes independently of its inhibitory action on lipid peroxidation.View full abstractDownload PDF (203K) -
Kouichi TAKEUCHI, Miki KOGURE, Takao HASHIMOTO1987 Volume 43 Issue 3 Pages 267-275
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of guanabenz, guanfacine and clonidine on α-adrenoceptors were investigated in isolated rat vas deferens and rabbit aortic strip. All 3 drugs at low concentrations (10-9-10-8 M) caused inhibition of twitch responses of the rat vas deferens induced by nerve stimulation. These effects were competitively antagonized by yohimbine. Guanfacine and clonidine at relatively high concentrations (10-6-10-4 M) produced contractions of the rat vas deferens which were antagonized by prazosin. These contractile responses were not much affected by denervation. Prazosin-sensitive contractions by guanfacine and clonidine were also observed in the rabbit aortic strip, which were not affected by reserpine pretreatment. In both tissues, the intrinsic activity of guanfacine was almost identical to that of norepinephrine, whereas that of clonidine was less than one half. Guanabenz and clonidine showed a competitive antagonistic effect against norepinephrine and phenylephrine in both the rat vas deferens and rabbit aorta, the antagonisms being similar in potency. The results indicate that all 3 drugs are potent agonists on the presynaptic α2-adrenoceptor. In contrast, on the postsynaptic α1-adrenoceptor, guanfacine and guanabenz showed only agonistic and antagonistic actions, respectively, whereas clonidine exhibited partial agonistic characteristics.View full abstractDownload PDF (507K) -
Nobuo KUBO, Osamu SHIRAKAWA, Takayoshi KUNO, Chikako TANAKA1987 Volume 43 Issue 3 Pages 277-282
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSQuantitative evaluation of antimuscarinic effects of antihistamines (H1and H2-receptor antagonists) was carried out using a receptor-binding assay. The inhibition constants (K1 values) of twenty seven H1-receptor antagonists, one related antidepressant and three H2-receptor antagonists at H1-receptors and muscarinic receptors in the bovine cerebral cortex were determined. All the H2receptor antagonists examined showed very low affinity for the muscarinic receptors. On the other hand, some H1-receptor antagonists (mequitazine, cyproheptazine, clemastine, diphenylpyraline, promethazine, homochlorcyclizine and alimemazine) had high affinity for the muscarinic receptors (K1=5.0-38 nM). Another group of H1 -receptor antagonists (mepyramine, terfenadine, metapyrilen, azelastine, hydroxyzine and meclizine) had low affinity for the muscarinic receptors (K1=3, 600-30, 000 nM). Thus, a broad range of antimuscarinic potencies among the antihistamines was demonstrated. These results should provide helpful information with regard to the clinical and experimental use of antihistamines.View full abstractDownload PDF (305K) -
Tetsu HAYASHI, Mineo KUNIHARA, Sakutaro TADOKORO1987 Volume 43 Issue 3 Pages 283-290
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSMale rats of the Wistar strain were repeatedly given methamphetamine (MAP) at 0.5 mg/kg, s.c., 10 times at a fixed interval of 4 days in different environmental situations. The effects of MAP administration on ambulatory activity and neurochemical parameters in the brain were investigated. MAP (0.5 mg/kg) markedly increased ambulatory activity. The ambulation-increasing effect of MAP was progressively enhanced without accompanying stereotyped behaviors when the drug was repeatedly given in the activity cage. The once enhanced effect was considered to be irreversible. In addition, the pretreatment with MAP in the activity cage produced a decrease in the maximum density of 3H-spiperone binding sites in the striatum and that of 3H-WB4101 binding sites in the cortex and hippocampus, with decreases in catecholamine and increases in its metabolites. However, the enhancement of the ambulation-increasing effect of MAP and changes in the binding sites or catecholamine metabolism were scarcely observed when the drug was repeatedly given to the rats in the narrow cage where horizontal ambulation of the animals was strongly impaired. These results suggest that the enhancing effect of MAP is closely related to the environmental situations to which the animals have been exposed to under the drug effect. Moreover, it is indicated that there is a correlation between the enhancement of the ambulation-increasing effect of MAP and changes in the neurochemical parameters. The enhancing effect of MAP is supposed to have been partially caused by changes in cerebral catecholaminergic systems, in particular an increase in catecholamine turnover.View full abstractDownload PDF (525K) -
Haruko KAMEDA1987 Volume 43 Issue 3 Pages 291-299
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe responses of guinea pig central and peripheral airways to labetalol (both α- and β-adrenoceptor blocker with intrinsic sympathomimetic activity) were studied using in vivo and in vitro preparations of the trachea and lung strips. The ventilation overflow enhanced by infusion of histamine in anesthetized guinea pigs was much more aggravated by labetalol and propranolol. The β-adrenoceptor blocking potency of labetalol and propranolol was not significantly different between the in vitro tracheal preparations and the lung strips. Isoproterenol and salbutamol relaxed the tracheal preparations more markedly than they did the lung strips. Histamine and acetylcholine contracted the lung strips more remarkably than they did the trachea. Labetalol relaxed the trachea more markedly than it did the lung strips by its intrinsic sympathomimetic activity. These results suggest that the peripheral airways are more sensitive to constrictors and the central airways are more sensitive to relaxants such as β-stimulants, and that the different responsiveness between the two airways to labetalol and histamine might have produced the different in vivo observations.View full abstractDownload PDF (450K) -
Hidetada KOMATSU, Masami KOJIMA, Naoyuki TSUTSUMI, Arao UJIIE, Shigeru ...1987 Volume 43 Issue 3 Pages 301-308
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSSlow reacting substance of anaphylaxis (SRS-A) has been shown to be one of the major mediators in hypersensitive reactions and to be composed of leukotriene (LT) C4, LTD4 and LTE4. In the present study, we examined the properties of SRS-A released from sensitized guinea pig lungs by antigen and SRS released from rat peritoneal exudate cells and from human leucocytes by ionophore A23187 (0.5 and 0.2 μg/ml, respectively). By the incubation with SRS-A, SRS and LTs with arylsulfatase (type V) in pH 5.7 buffered solution at 37°C for 30 min, SRS-A and LTD4 were greatly inactivated and rat SRS was slightly inactivated, but human SRS and LTC4 were not inactivated at all. The same results were obtained when aminopeptidase was used in place of arylsulfatase. Moreover, when SRS-A, LTC4 and LTD4 were incubated with 0.02 mg/ml of γ-glutamyltranspeptidase (γ-GTP) pH 8.0 buffered solution at 37°C for 30 min, the activities of SRS-A and LTD4 were slightly decreased, but those of SRS and LTC4 were obviously potentiated. On the other hand, incubation with a large amount of γ-GTP (0.2 mg/ml) a dose at which this enzyme preparation showed clear aminopeptidase activity, SRS-A, SRS, LTC4 and LTD4 were obviously inactivated. In addition, we found a peak of LTD4 in guinea pig SRS-A, that of LTC4 in human SRS, and that of LTC4 in rat SRS on high performance liquid chromatograms. From these results, we demonstrated that guinea pig lung SRS-A is mainly composed of LTD4, human leukocyte SRS is mainly LTC4, and rat peritoneal SRS is composed of both LTC4 and LTD4. The inactivation of LTD4 and SRS-A by arylsulfatase may be due to aminopeptidase contamination in the enzyme preparation.View full abstractDownload PDF (385K) -
Showa UEKI, Shigenori WATANABE, Tsuneyuki YAMAMOTO, Yasufumi KATAOKA, ...1987 Volume 43 Issue 3 Pages 309-326
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSBehavioral effects of zopiclone were investigated in mice and rats and compared with the data on diazepam, nitrazepam and flurazepam. The electro-encephalographic effect of the drug was also examined in unanesthetized rabbits with chronic electrode implants and compared with that of diazepam. The present results indicate that zopiclone possesses pharmacological properties qualitatively similar to benzodiazepines, which are characterized by potent anticonflict and antiaggressive effects and much weaker anticonvulsant, muscle relaxant, ataxiogenic, sedative and anesthesia potentiating effects; the properties of this drug were compared with those of diazepam, nitrazepam and flurazepam. Zopiclone suppressed the EEG arousal responses and inhibited afterdischarges induced by electrical stimulation of the hippocampus and amygdala. The effects of zopiclone on EEG and afterdischarges were approximately 1/10 those of diazepam.View full abstractDownload PDF (879K) -
Hiroshi WATANABE, Hiroshi SUDA, Shun-ichi SEKIHARA, Yasuyuki NOMURA1987 Volume 43 Issue 3 Pages 327-330
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTo clarify if dopamine (DA) synthesis is regulated by D-1 DA receptors located on dopaminergic nerve terminals in the striatum, we investigated effects of D-1 DA receptor agonist and antagonist on striatal 3, 4-dihydroxyphenylalanine (DOPA) accumulation induced by γ-butyrolactone in mice treated with an amino acid decarboxylase inhibitor. SKF 38393, a D-1 agonist, did not affect DOPA accumulation, whereas apomorphine that stimulates both D-1 and D-2 receptors inhibited the accumulation. SCH 23390, a D-1 antagonist, did not antagonize apomorphine-induced inhibition of DOPA accumulation, while YM-091 51-2, a D-2 antagonist, reversed it. These results suggest that D-1 type of DA autoreceptors is not involved in the inhibition of in vivo DA synthesis.View full abstractDownload PDF (213K) -
Nobuyuki OGAWA, Syunji YOKOTA, Hiroshi ONO1987 Volume 43 Issue 3 Pages 331-334
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSAn intra-arterial infusion of a calmodulin inhibitor trifluoperazine (3 mg/min) or chlorpromazine (5 mg/min) caused obvious inhibition of autoregulation of renal blood flow in dogs. Simultaneous infusion of CaCl2 (30 mg/min) or Ca channel activator BAY K 8644 (5 μg/min) with these calmodulin inhibitors reduced renal blood flow, but could not block the inhibitory activity of calmodulin inhibitors on the autoregulation. The present experiment shows the contribution of the Ca-calmodulin system to the mechanism of autoregulation of renal blood flow.View full abstractDownload PDF (236K)
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