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Volume 53 (1990)
- Issue 4 Pages 419-
- Issue 3 Pages 285-
- Issue 2 Pages 135-
- Issue 1 Pages 1-
Volume 53, Issue 3
Displaying 1-16 of 16 articles from this issue
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Chuan Chiung CHANG, Lih Chu CHIOU, Lin Lin HWANG, Chen Yen HUANG1990 Volume 53 Issue 3 Pages 285-292
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSThe effects of Mn2+, neomycin and four organic Ca2+-channel antagonists (OCA): nicardipine, nifedipine, diltiazem and verapamil on the neuromuscular blocking activities of tubocurarine, succinylcholine (SCh), decamethonium and neomycin were studied in isolated mouse phrenic nerve-diaphragm preparations. The effective concentration of SCh for 50% inhibition (IC50) of single indirect twitch responses were reduced markedly by more than 3-fold when the preparations were pretreated with OCA at 10 μM; the latter alone did not appreciably affect the indirect twitch response or the amplitude of miniature endplate potentials. The neuromuscular blocking effect of decamethonium was also enhanced synergistically by OCA to a similar extent. On the other hand, under the comparable condition, the combined uses of OCA plus tubocurarine or neomycin, neomycin plus tubocurarine or SCh, and Mn2+ plus tubocurarine, SCh or neomycin all resulted in insignificant potentiation. These results suggest that OCA have a specific effect to enhance the agonist effect of depolarizing agents on nicotinic acetylcholine receptors. Nicardipine at 2 μM non-competitively inhibited depolarizations of endplates elicited by SCh and decamethonium and abolished them completely at 10 μM nicardipine. The IC50's in inhibiting endplate potentials and miniature endplate potentials by SCh and decamethonium were also reduced 2 to 3.5-fold by nicardipine. It is inferred that OCA are endowed with a unique capability to allosterically affect the postsynaptic nicotinic acetylcholine receptor, promoting its desensitization liability, hence synergistic interaction with depolarizing agents. Presynaptic effects of OCA are probably not involved.View full abstractDownload PDF (474K) -
Yoshio TSUCHIYA, Tomokazu HOSOKAWA, Yutaka KASUYA1990 Volume 53 Issue 3 Pages 293-300
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSThe effects of ouabain on the smooth muscles of the airway were investigated in anesthetized, paralyzed and artificially ventilated mongrel dogs. Ouabain (30 μg/kg, i.v.) caused a constriction of the tracheal smooth muscle which was followed by bradycardia. When ouabain was infused at a rate of 2 μg/kg/min (i.v.), the tracheal constriction was induced by a total dose of 45.0±5.5 μg/kg, while the bradycardia appeared with a total dose of 54.4±6.1 μg/kg. The ouabain-induced tracheal constriction was inhibited by bilateral vagotomy. The tracheal constriction induced by La. infusion of 10 μM ouabain into the bilateral cranial thyroid arteries was inhibited by bilateral vagotomy, but it was not completely blocked. With bilateral vagotomy, the tracheal constriction induced by i.a. infusion of ouabain was unaffected by 3 μM hexamethonium, but it was significantly inhibited by 1 μM atropine. These results suggest that ouabain may induce tracheal constriction by a neurogenic action in addition to its action via the augmentation of the vagal reflex, and the neurogenic action of ouabain may be related, in large part, to the release of acetylcholine from the presynapses of vagus nerves in dogs.View full abstractDownload PDF (387K) -
Yoshio TSUCHIYA, Tomokazu HOSOKAWA, Yutaka KASUYA1990 Volume 53 Issue 3 Pages 301-309
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSThe effect of ouabain on the cholinergic neurotransmission of the trachea was investigated using isolated tracheal strips in dogs. Tracheal strips without epithelium were suspended in organ chambers filled with modified KrebsHenseleit solution. Ouabain (3×10-7-10-5 M) concentration-dependently caused a slow sustained tracheal contraction. The contractile response was significantly inhibited by 10-6 M atropine and was enhanced by 10-8 M physostigmine. The ouabain-induced tracheal contraction was unaffected by 10-7 M tetrodotoxin, but was significantly reduced by 10-3 M hemicholinium-3. In superfusion experiments, ouabain (10-5 M) produced an increase in the ACh release. Superfusion with Ca++-free solution almost eradicated the ACh release and abolished the tracheal contraction induced by ouabain. ω-Conotoxin (5×10-8 M), but not nicardipine (10-6 M), inhibited significantly the increase in ACh release induced by ouabain. These results suggest that the ouabain-induced tracheal contraction may be mainly due to acceleration of presynaptic ACh release by enhancing the influx of Ca++, and the Ca++ entry may occur through the N-type Ca++ channels in the canine airway presynaptic site.View full abstractDownload PDF (418K) -
Xue-Hui ZHAO, Akira AWAYA, Hisashi KOBAYASHI, Toshio OHNUKI, Yukiko TO ...1990 Volume 53 Issue 3 Pages 311-319
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSSuperoxide dismutase (SOD) activity, malondialdehyde (MDA) content and monoamine oxidase B (MAO-B) activity were measured in the brain, liver and kidney of a normal aging strain (R/1) and an accelerating aging strain (P/8) senescence-accelerated mice (SAM) at 9-10 months of age, and the effects of facteur thymique sérique (FTS) were examined. The activity of Cu, Zn-SOD in the kidney and MAO-B in the liver was significantly low and high in SAM-P/8 compared to SAM-R/1. FTS enhanced the activity of Mn-SOD and Cu, Zn-SOD in the kidney of SAM-P/8 and Cu, Zn-SOD activity in the brain of both SAM-P/8 and SAM-R/1. It decreased the activity of MAO-B in the liver and the contents of malondialdehyde (MDA) in the brain and kidney of SAM-P/8. Thus, FTS affects the biochemical factors related to senescence in SAM-P/8, a particular senescent animal model, and may thus possibly be effective as an anti-senescent medicine.View full abstractDownload PDF (434K) -
Akira HIROSE, Terufumi KATO, Yukihiro OHNO, Hiroshi SHIMIZU, Hiroyasu ...1990 Volume 53 Issue 3 Pages 321-329
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSPharmacological studies were undertaken to clarify the profile of cis-2-(4-(4-(1, 2-benzisothiazol-3-yl)-1-piperazinyl) butyl) hexahydro-1H-isoindole-1, 3-(2H)-dione hydrochloride (SM-9018), a new neuroleptic drug. SM-9018 had very high binding affinities for both 5-hydroxytryptamine2 (5-HT2) and dopamine2 (D2) receptors, unlike many other neuroleptics. SM-9018 also strongly inhibited 5-HT2 receptor-mediated behavior such as tryptamine-induced clonic seizure and D2 receptor-mediated behavior such as methamphetamine-induced hyperactivity, apomorphine-induced stereotypy and climbing behavior. SM-9018 possessed only a weak cataleptogenic activity, which may be clinically related to extrapyramidal side effects, despite its potent D2 antagonistic activity. Moreover, SM-9018 induced weak central depressant effects such as inhibition of spontaneous locomotor activity and motor coordination, as compared with classical neuroleptics (haloperidol and chlorpromazine). These results suggest that SM-9018 is a new neuroleptic drug with both potent 5-HT2 and D2 antagonistic activities and with low cataleptogenic and central depressant activities.View full abstractDownload PDF (519K) -
Akira FUJII, Sumi KOBAYASHI, Noboru KUBOYAMA, Yoko FURUKAWA, Yoshiaki ...1990 Volume 53 Issue 3 Pages 331-337
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSChronically diabetic rats prepared by a single i.v. Injection of streptozotocin were used to study whether royal jelly (RJ) possesses a hypoglycemic reaction and whether it can augment wound healing. Oral RJ administration of 10, 100 and 1000 mg/kg/day did not show any insulin-like activity (the hypoglycemic reaction). RJ, however, showed some anti-inflammatory activity by decreasing exudation and collagen formation in granulation tissue formation in the cotton pellet method. RJ also shortened the healing period of desquamated skin lesions. Thus, RJ possesses an anti-inflammatory action and is able to augment wound healing, but does not have an insulin-like action in streptozotocin-diabetic rats.View full abstractDownload PDF (409K) -
Yasuko KARASAWA, Hiroaki ARAKI, Shigeru OKUYAMA, Hironaka AIHARA, Susu ...1990 Volume 53 Issue 3 Pages 339-346
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSWe examined the characteristics of cerebral ischemia-induced behavioral deficit in the passive avoidance task and the effect of minaprine and other cytoprotective drugs on passive avoidance deficit induced by cerebral ischemia in Mongolian gerbils. Severe impairment of passive avoidance was apparent when the duration of the ischemia exceeded 2 min. Histopathological ischemic neuronal damage in CA1 neurons at 7 days after occlusion was also induced when the ischemia was over 2 min. Otherwise, although cerebral ischemia was carried out at 5 min, 2 hr, 5 hr or 24 hr after the training session, the passive avoidance deficit was produced 24 hr after the training session. When the training session was carried out 24 hr before the occlusion, minaprine, which was administered 30 min before the occlusion, led to a recovery of the response latency. Pentobarbital, diazepam and ethylapovincamine improved the passive avoidance deficit induced by 5-min bilateral carotid artery occlusion. On the other hand, the passive avoidance deficit was not ameliorated by Ca++-hopantenate, nicardipine and idebenone. The hippocampal damage at 7 days after occlusion was prevented by the drugs that ameliorated the passive avoidance deficit. The relationship between passive avoidance deficit and CA1 neuronal death in the hippocampus induced by cerebral ischemia warrants further attention.View full abstractDownload PDF (570K) -
Ryoji KOJIMA, Mikio ITO, Yoshio SUZUKI1990 Volume 53 Issue 3 Pages 347-358
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSWe examined the protective effect of inositol hexasulfate (IS6) against tobramycin (TOB)-induced nephrotoxicity. In the electrophoretic analysis, TOB alone and IS6 alone were observed as single spots on the cathode and anode sides, respectively. However, in the mixture of TOB and IS6 preincubated at 37°C for 3 hr, the tailing of the spots of TOB and IS6 were observed from the origin to the cathode and the anode sides, respectively, and the overlapping of the spots of TOB and IS6 was recognized at the origin. These results indicated that TOB directly interacted with IS6 in vitro. Assay of TOB binding to rat kidney brush border membranes (BBMs) indicated that IS6 inhibited the binding of TOB to BBMs through an interaction of TOB and IS6. No significant reduction in intrarenal TOB level was observed in the rats given TOB (90 mg/kg, s.c.) and IS6 (153 or 610 mg/kg, s.c.). However, the treatment of rats with a combination of TOB and IS6 reduced the degree of necrosis of renal tubular cells and also suppressed the increases in urinary protein, urinary enzyme activities, blood urea nitrogen and plasma creatinine induced by TOB. Additionally, we detected a complex of TOB and IS6 in the urine of rats given both compounds simultaneously. These results indicate that IS6 protects against TOB-induced nephrotoxicity and that the protective action of IS6 may be due to the inhibition of TOB binding to BBMs through an interaction of TO B with IS6.View full abstractDownload PDF (1058K) -
Issei TAKAYANAGI, Ken-ichi KAWANO, Katsuo KOIKE1990 Volume 53 Issue 3 Pages 359-366
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSTo study the effect of aging on the β-adrenergic receptor potency of isoprenaline, tracheas from 3-, 6-, 10-, 40 and 100-week-old guinea pigs were used as test tissues. The pD2 values (potency) of isoprenaline increased with age in tracheas treated with corticosterone, but decreased in untreated tracheas. The pA2 value of propranolol against isoprenaline estimated in the treated tracheas did not change with age. Specific binding of [3H]-dihydroalprenolol to the microsomal fractions from the tracheal muscles from 6-, 10- and 40-week-old guinea pigs was analyzed with Scatchard plots. The capacity of maximum binding sites of [3H]-dihydroalprenolol increased with increasing age, while its dissociation constant did not change. Age-related increase in the potency of isoprenaline in the tracheas treated with corticosterone is considered to be due to the increase in the total amount (density) of β-adrenoceptors. However, the potency of the drug in untreated tracheas decreased with age. These results suggest that extraneuronal uptake plays an important role in the β-adrenergic action of isoprenaline in older (40 and 100 weeks) guinea pigs.View full abstractDownload PDF (447K) -
Hiroshi IZUMI, Shoryo HAYASHI1990 Volume 53 Issue 3 Pages 367-374
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSSubcutaneous (s.c.) injection of Hoe 498, an angiotensin converting enzyme (ACE) inhibitor, at the doses of 0.1, 0.5, 1.0 and 4.0 mg/kg produced a dose-related inhibition of compound 48/80-induced hypovolemic thirst in rats. A significant time-response relationship was observed between the pretreatment time of Hoe 498 at a dose of 4.0 mg/kg and the inhibition of compound 48/80-induced water intake. Nearly 90% of plasma ACE activity was inhibited by Hoe 498 at all doses used, and this inhibition at the dose of 4.0 mg/kg of Hoe 498 continued for more than 4 hr. Intracerebroventricular (i.c.v.) or s.c. injection of Hoe 498 in doses ranging from 0.5 to 20 μg comparably inhibited plasma ACE activity in a dose-dependent manner. The compound 48/80-induced water intake was significantly reduced by i.c.v. injection of Hoe 498 (20 μg) 30 min after compound 48/80 administration, but not reduced when the drug was given 15 min prior to injection of dipsogen. The inhibition of water intake by Hoe 498 seems to be dependent on the dose and time between administration of Hoe 498 and compound 48/80. The present data suggest that brain ACE is more involved in compound 48/80-induced water intake than peripheral systemic ACE.View full abstractDownload PDF (430K) -
Yoshinobu AKIMOTO, Kazuyoshi KURAHASHI, Motohatsu FUJIWARA1990 Volume 53 Issue 3 Pages 375-380
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSThe effects of extraneuronal accumulation of isoprenaline on the level of cAMP in perfused rat hearts were investigated. When catechol-0-methyl transferase (COMT) was intact, perfusion with isoprenaline (10-6 M) for 5 min and 30 min (low accumulation of isoprenaline in the heart) enhanced the cAMP level. Propranolol (10-6 M) significantly decreased the high level of cAMP produced by the perfusion with isoprenaline for 5 min and 30 min (low accumulation of isoprenaline). When COMT was inhibited by tropolone, perfusion with isoprenaline (10-6 M) for 5 min (slight accumulation of isoprenaline in the heart) slightly increased the level of cAMP, while perfusion for 30 min (high accumulation of isoprenaline in the heart) did not increase the level of cAMP. Propranolol (10-6 M) significantly decreased the cAMP level produced by 5 min perfusion with isoprenaline, but did not change the level by 30 min perfusion. The perfusion length (5 min and 30 min) and COMT inhibition by tropolone (10-4 M) in the absence of isoprenaline did not affect cAMP levels. These results suggest that extraneuronally accumulated isoprenaline may inhibit the adenylate cyclase in perfused rat hearts.View full abstractDownload PDF (365K) -
Katsuhiko NOGUCH, Takayuki KATO, Noriko KINJO, Hidehiko MOROMIZATO, Ma ...1990 Volume 53 Issue 3 Pages 381-391
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSEffects of arotinolol, a combined alpha- and beta-adrenoceptor blocking agent, on regional myocardial dysfunction produced by severe coronary stenosis in anesthetized dogs were examined and compared with those of labetalol and propranolol. Doses of these three antagonists were selected to produce a comparable degree of the negative chrono- and inotropic effect but a different potency of alpha-adrenoceptor blockade (labetalol>arotinolol). Regional myocardial function measured as segment shortening (%SS) was decreased to around 2-3% by constriction of the left circumflex coronary artery (LCX), and then drug or saline was administered i.v. The stenosis of LCX was released 30 min after the administration. No significant alteration in hemodynamic and contractility parameters was seen as compared to the predrug value up to at least 30 min after saline i.v. Arotinolol and propranolol both reduced heart rate and peak positive left ventricular dP/dt (LVdP/dt) without a significant change in LCX flow. Concomitantly, %SS distal to a coronary stenosis was significantly improved by arotinolol and propranolol. On the other hand, labetalol significantly reduced LCX flow probably due to systemic hypotension and failed to improve %SS in the ischemic area, although the agent markedly decreased heart rate and LVdP/dt. These results indicate that arotinolol improves impaired regional myocardial function distal to a coronary stenosis in a similar manner with propranolol.View full abstractDownload PDF (546K) -
Kayo AKIYAMA, Den'etsu SUTOO, David G. REID1990 Volume 53 Issue 3 Pages 393-401
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSOur previous reports based on pharmacological and histochemical evidence suggest that calcium and cadmium can both activate calmodulin (CaM)-dependent functions. The study reported here was carried out to explain these observations in molecular terms, using 400 MHz 1H-NMR. Changes in the spectrum of bovine brain CaM induced by 0 to 4 molar equivalents of calcium and cadmium were practically the same. In particular, the chemical shifts and line shape of signals due to Tyr-138, Phe-65, Phe-89 and Tml-115 were similarly affected by either ion. In addition, the effects of N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7, a CaM antagonist) on the phenylalanine aromatic regions, methionine methyl regions and high-field methyl regions of the spectra of both calcium and cadmium-saturated proteins were practically identical. The effect of W-7 on calcium- and cadmium-saturated CaM was reflected in changes in the signals of Ile-27, Phe-68, Phe-92, Ile-100 and Val-142, as well as Met-71, Met-72, Met-76, Phe-89 and Phe-141. The results show that cadmium binds to all calcium-binding sites of CaM, and induces conformational changes that are as extensive as those brought about by calcium. W-7 also inhibits CaM activation by calcium and cadmium Combined with our previous toxicological evidence, these results suggest that cadmium binds indiscriminately to CaM and that subsequent activation or modulation of CaM-dependent functions is confused as a result. This may be a mechanism contributing to cadmium poisoning.View full abstractDownload PDF (435K) -
Yuki JIKOH, Hiroaki NISHIO, Kimiko OKUGAWA, Tomio SEGAWA1990 Volume 53 Issue 3 Pages 403-410
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSPossible involvement of protein kinases in the serotonin (5-HT) transport system in platelets and the inhibitory effect of concanavalin A (Con A) on platelet 5-HT uptake were investigated. Staurosporine and K-252a, highly active inhibitors of protein kinases, did not inhibit 5-HT transport, but they antagonized the inhibitory effect of Con A on 5-HT uptake. KT5720, a protein kinase A inhibitor that has no effect on protein kinase C, neither affected 5-HT transport nor antagonized the inhibitory effect of Con A on 5-HT uptake. The Con A effect on 5-HT uptake was also antagonized by LaCl3, a Ca++ entry blocker. When the activity of Ca++ transport into platelets was estimated, Con A was shown to have a stimulative effect, which was antagonized by α-methyl-D-mannoside, a specific antagonist of Con A binding to cell membrane glycoproteins. Furthermore, Con A was shown to stimulate the protein kinase C activity of platelets, which phosphorylates a 40-kDa platelet protein; the Con A effects were antagonized by α-methyl-D-mannoside, staurosporine and K-252a, but not by KT5720. We suggest that the activation of protein kinase C and phosphorylation of 40-kDa protein might be involved in the inhibitory effect of Con A on platelet 5-HT transport.View full abstractDownload PDF (395K) -
Kazuaki KAWASHIMA, Hiroaki ARAKI, Hironaka AIHARA, Susumu OTOMO1990 Volume 53 Issue 3 Pages 411-413
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSWe examined the effects of minaprine and sulpiride injected into the medial amygdaloid nucleus on the duration of immobility in rats forced to swim. Minaprine (50 μg/μl) significantly reduced the duration of immobility, while sulpiride (50 μg/μl) remarkedly enhanced it. These results suggest that the medial amygdaloid nucleus might be involved in the suppressive effect of minaprine on the duration of immobility, as was seen with the tricyclic antidepressants. The pattern of behavior seen with sulpiride administrations differs considerably from that seen with the tricyclic antidepressants.View full abstractDownload PDF (157K) -
Yutaka GOMITA, Yasuyuki ICHIMARU, Katsushi FURUNO, Yasunori ARAKI1990 Volume 53 Issue 3 Pages 414-418
Published: 1990
Released on J-STAGE: July 11, 2006
JOURNAL FREE ACCESSIn rats with electrocoagulation of the unilateral subtantia nigra (SN), methamphetamine at doses of 2.5 and 5 mg/kg, i.p., induced ipsilateral turning towards the lesioned side and caused an imbalance of the regional cerebral glucose utilization (CGU) in the caudate-putamen (CP), frontal cortex (FC) and ventromedial thalamic nucleus (VMT); i.e., showing a higher contralateral CGU as compared with the SN lesioned side. These results induced in unilateral SN-lesioned rats may be accompanied by an imbalance of neural activity in CP, FC and VMT of these rats.View full abstractDownload PDF (277K)
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