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Volume 85 (2001)
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Volume 85, Issue 3
Displaying 1-18 of 18 articles from this issue
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Reviews
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Satoshi Shuto, Kiyonori Yoshii, Akira MatsudaSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 207-213
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSWe have found that milnacipran, a clinically useful antidepressant due to its inhibition of the re-uptake of serotonin (5-HT) and noradrenaline, is also a non-competitive NMDA-receptor antagonist. Based on the cyclopropane structure of milnacipran, conformationally restricted analogs were designed and synthesized. Of these analogs, (1S,2R)-1-phenyl-2-[(S)-1-aminopropyl]-N,N-diethylcyclopropanecarboxamide (PPDC) is 30-fold stronger than milnacipran as an NMDA-receptor antagonist with virtually no inhibitory effect on the neurotransmitter re-uptake. PPDC was identified as a new class of NMDA-receptor antagonist because it has a mode of action different from that of the previous antagonists; it selectivly binds the GluRε3/GluRζ1 and GluRε4/GluRζl subtype receptors in an agonist-independent allosteric manner. Functional assays of PPDC with the Xenopus oocytes system and cultured mouse neurons under voltage-clamp conditions confirmed that it acts as a potent NMDA-receptor antagonist. PPDC effectively protected against NMDA-induced neurotoxicity in both cultured mouse cerebral cortex and delayed neuronal death in a gerbil ischemic model. It was also active in a reserpine-treated mouse Parkinsons disease model. Thus, PPDC may be a candidate for a clinically useful NMDA-receptor antagonist, since the development of previous NMDA-receptor antagonists as drugs has been hindered by various undesirable side effects.View full abstractDownload PDF (215K)
Full papers
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Katsuyuki Mishima, Hitomi Otani, Takatoshi Tanabe, Hiroshi Kawasaki, A ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 214-226
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSThe sympathetic nervous system has been indicated to influence the severity of inflammatory disease including rheumatoid arthritis. In this study, we elucidated the effects of catecholamine on the synovial cell populations. Stimulation with epinephrine or norepinephrine for 1 - 2 weeks dose- and time-dependently increased the number of synovial A (macrophage-like) cells but decreased that of B (fibroblast-like) cells. These responses in A and B cells were inhibited by the α2-antagonist yohimbine, the G-protein inactivator pertussis toxin and the phospholipase C (PLC) inhibitor U-73122. Furthermore, the protein kinase C (PKC) inhibitor calphostin C and mitogen-activated protein (MAP) kinase inhibitors PD98059 and wortmannin also abolished the norepinephrine effects on A and B cell numbers. In A cells cloned from an A and B cell mixture, norepinephrine also increased the cell number. In immunoblotting and immunocytostaining analyses, among the PKC isozymes, only PKC βII immunoreactivity was observed in the cytoplasm of unstimulated A and B cells. After α2-adrenoceptor stimulation, PKC βII immunoreactivity increased in the plasma membranes of both A and B cells with decreases in the cytoplasm. These findings indicated that α2-adrenoceptor stimulation of type A and B synoviocytes produced an increase and a decrease in the respective cell number, probably through Gi-coupled PLC activation and the resulting stimulation of the PKC βII/MAP kinase.View full abstractDownload PDF (1215K) -
Fusako Takayama, Toru Egashira, Yasumitsu YamanakaSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 227-233
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSTo establish a simple screening system for estimating efficacy of an agent for an oxidative-related lesion, we investigated the damage in isolated rat hepatocytes exposed to 75 μM tert-butyl hydroperoxide (t-BuOOH) and then subsequently incubated the cells in fresh medium. By electron spin resonance spectroscopy analysis using 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), DMPO adducts of tert-butoxyl radicals and carbon center radicals were detected during the t-BuOOH exposure, and DMPO-OH formation was detected after t-BuOOH removal. In t-BuOOH-exposed cells, the level of phosphatidylcholine hydroperoxide (PCOOH), a peroxidative product of biomembranes in the hepatocytes, and the leakage of enzymes into the culture medium were significantly increased. An increase in acid phosphatase (AP) activity representing lysosome destabilization preceded the aspartate oxoglutarate aminotransferase (AST), alanine oxoglutarate aminotransferase (ALT) and lactate dehydrogenase (LDH) leakage. Ninjin-yoei-to added to the culture medium following the t-BuOOH exposure significantly inhibited the PCOOH formation and the leakage of AP, AST, ALT and LDH, concentration-dependently. Ninjin-yoei-to at 1 mg/ml in culture medium completely diminished these increases in enzyme activities down to the background levels found in control experiments and this reduction was greater than the most effective α-tocopherol concentration of 20 μmol/ml. Considering all of these results, it is likely Ninjin-yoei-to may exert its protective effect by anti-oxidative action and membrane stabilization.View full abstractDownload PDF (262K) -
Chiu-Yin Kwan, Paul H.M. Harrison, Petra A. Duspara, Edwin E. DanielSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 234-240
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSA newly discovered antifungal agent, pramanicin, within the therapeutically effective concentration range (4 - 100 μM), inhibits the tone of phenylephrine (PE)-precontracted dog carotid arterial rings in a concentration-dependent manner and leads to gradual development of relaxation. However, pramanicin had no effect on rings precontracted with 100 mM KCl or on endothelium-denuded rings. Thus, inhibition by pramanicin of PE-induced contraction was endothelium-dependent. Preincubation of 100 μM pramanicin with carotid arterial rings for 30 min did not significantly affect the concentration-contraction response to PE, but almost completely inhibited the endothelium-dependent relaxation response to subsequent addition of 3 μM carbachol or 100 μM pramanicin. This irreversible inhibition of endothelium-dependent relaxation, which is independent of extracellular Ca2+, suggests possible endothelial cell damage by pramanicin. Pretreatment of the endothelium-intact vascular rings with L-NG-nitro-arginine (100 μM) inhibited the relaxation of PE-precontracted rings induced by 3 μM carbachol or 100 μM pramanicin, suggesting that the generation of nitric oxide (NO) in endothelial cells mediates the slow vascular relaxation induced by pramanicin. We conclude that pramanicin has little direct effect on the contractility of smooth muscle cells, but causes an initial slow endothelium-dependent, NO-mediated vascular relaxation. This is followed by a cytotoxic effect on vascular endothelial cells, eventually resulting in the loss of vasorelaxant function.View full abstractDownload PDF (203K) -
Prasannajit Dutta, Deanne E. Ryan, Reza TabrizchiSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 241-249
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSAdministration of bacterial endotoxin (lipopolysaccharide, LPS) intravenously has been noted to produce a shock state, which is characterized by hypotension and mutli-organ system failure. The aim of the present investigation was to (a) examine the influence of rolipram on hemodynamics, plasma levels of tumor necrosis factor-α (TNF-α) levels, and production of inducible nitric oxide synthase (iNOS) in the lungs, ex vivo, in LPS-treated rats, and (b) determine the cardiovascular effects of a selective α1-adrenoceptor agonist, methoxamine, in the absence or presence of rolipram in rats treated with LPS. Blood pressure, cardiac index, heart rate and arterial resistance were assessed in Long-Evans rats anesthetized with thiobutabarbital. Administration of LPS to animals resulted in a significant reduction in cardiac index over time. The administration of LPS to rats resulted in a substantial rise in the plasma levels of TNF-α. Furthermore, the injection of LPS resulted in a significant increase in the iNOS activity in the lungs. Pre-treatment with rolipram prevented the decline in cardiac index in animals that received LPS. Infusion of methoxamine into animals injected with rolipram and pre-treated with LPS did not result in significant changes in cardiac index. Pre-treatment with rolipram or dexamethasone in animals injected with LPS significantly prevented the rise in TNF-α when compared to the respective values in vehicle-treated animals. Our present observations support the view that the cardiac index can be maintained in animals treated with LPS independent of iNOS inhibition.View full abstractDownload PDF (222K) -
Naoki Kawada, Hiroyuki Tanaka, Toshiaki Takizawa, Takatoshi Yamada, Yo ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 250-259
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSThe participation of mast cells in the induction of antigen-induced airway inflammation and bronchial hyperresponsiveness (BHR) to acetylcholine (ACh) was investigated using pharmacological agents and mast cell-deficient rats (Ws/Ws). A significant increase in the number of leukocytes in bronchoalveolar lavage fluid (BALF) and bronchial responsiveness to ACh were observed 24 h after antigen (ovalbumin) challenge in sensitized Brown-Norway (BN) rats. Disodium cromoglycate and terfenadine did not inhibit antigen-induced airway inflammation and BHR in sensitized BN rats. In contrast, cyclosporin A (CyA), FK-506 and prednisolone significantly inhibited antigen-induced airway inflammation and BHR in sensitized BN rats. In addition, disodium cromoglycate, terfenadine and prednisolone, but not CyA and FK-506, inhibited homologous passive cutaneous anaphylaxis in rats. Furthermore, a significant increase in the number of leukocytes in BALF and BHR was also observed in Ws/Ws rats 24 h after inhalation of antigen; however, the magnitude of BHR in Ws/Ws rats was lower than that in the congenic rats. These findings suggest that mast cells play a partial role in the development of antigen-induced BHR in rats and that the induction of BHR is barely suppressed by mast cell stabilizing agents.View full abstractDownload PDF (527K) -
Ryuji Uchida, Jun Yamazaki, Satoru Ozeki, Kenji KitamuraSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 260-270
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSUsing a whole-cell patch-clamp technique, state-dependent inhibition of dihydropyridines (DHP)s was investigated on L-type channels in A7r5 cells. Cilnidipine, its derivatives (D-342 and D-69) and nimodipine inhibited the Ba2+ current. However, cilnidipine and D-342, but not D-69 or nimodipine, accelerated current decay. The apparent rank order for the effects on the DHP-sensitive decaying component was different from that obtained for inhibition of the peak current. The dissociation constants for cilnidipine in the resting and inactivated states were estimated to be 190 and 12 nM, respectively. Cilnidipine, but not other DHP derivatives, created a faster and voltage-independent component (τ = 37 ms). The linear relationship between the τ−1 of the current decay and the cilnidipine concentration provided a value of 471 nM for the dissociation constant in the open state, suggesting that the current decay is mediated by one-to-one lower affinity binding of cilnidipine molecules to their binding site. The present study demonstrates that structurally related DHPs act in distinct ways to inhibit the L-type channel in the resting, open and inactivated states. Cilnidipine and some related DHPs probably exert their blocking action on the open channel by binding to a receptor distinct from the known DHP-binding site.View full abstractDownload PDF (358K) -
Naotsugu Horikawa, Yoshikazu Kuribayashi, Natsuko Itoh, Mizue Nishioka ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 271-277
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSEndothelial cells play an important role in the physiologic homeostasis of the cerebral circulation. Previously, we showed that the Na+/H + exchanger (NHE) inhibitor SM-20220 (N-(aminoiminomethyl)-1-methyl-1H-indole-2-carboxamide methanesulfonate) improved ischemic brain injury. In this study, we investigated the effect of SM-20220 on cerebrovascular dysfunction after ischemia-reperfusion, focusing on the kinds of dysfunction that involved endothelial function. In cultured bovine brain microvascular endothelial cells (BBMCs), the IC50 value for the NHE activity of SM-20220 was 4 × 10−8 M. SM-20220 also reduced the cell injury induced by hypoxia/aglycemia-reoxygenation in BBMCs, with statistical significance at 10−7 M (P<0.05). Next, the effect of SM-20220 on disruption of the blood-brain barrier and cerebral blood flow were evaluated using transient middle cerebral artery (MCA) occlusion models. Intravenous infusion of SM-20220 (0.4 mg/kg per hour for 1 h) attenuated the extravasation of Evans blue, a blood-brain barrier disruption indicator, into cerebral tissue on the day after transient ischemia (P<0.05). The occlusion of the MCA decreased the cerebral blood flow in the MCA territory by about 20%, and only about 45% of the preischemic value was recovered at 1-h reperfusion. A bolus injection of SM-20220 (1 mg/kg, i.v.) improved the postischemic hypoperfusion by about 75%, without causing changes in the systemic blood pressure. These results indicate that the protective effect of NHE inhibitor on ischemic brain injury may be at least partially mediated by the prevention of endothelial dysfunction.View full abstractDownload PDF (533K) -
Takashi Fujita, Toru Meguro, Nobuo Izumo, Chigusa Yasutomi, Ryo Fukuya ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 278-281
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSATDC5 cells were employed to examine how inorganic phosphate (Pi) influences chondrocytic bone formation. 1) Pi (3 - 30 mM) plus ascorbic acid (50 μg/ml) dose-dependently accelerated proliferative differentiation and mineralization of ATDC5. 2) Northern blot analysis revealed that 10 mM Pi suppressed expression of type II collagen and PTH (parathyroid hormone) / PTH-related peptide (PTHrP) receptor, while it accelerated type X collagen expression. 3) Pi (3 - 30 mM) dose-dependently increased luciferase activity in the cells transfected with 3000 bp type X collagen promoter fused to the luciferase gene. The results suggest a regulatory role of Pi in endochondral osteogenesis.View full abstractDownload PDF (427K) -
Takashi Endoh, Atsushi Tajima, Naoki Izumimoto, Tomohiko Suzuki, Akiyo ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 282-290
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSTRK-820 ((−)-17-cyclopropylmethyl-3,14b-dihydroxy-4,5a-epoxy-6b-[N-methyl-trans-3-(3-furyl)acrylamide]morphinan hydrochloride) has been shown to be a potent opioid κ-receptor agonist with pharmacological properties different from those produced by κ1-opioid receptor agonists in rodents. To ascertain whether or not these properties of TRK-820 would be extended to primates, the antinociceptive effect of TRK-820 was evaluated in cynomolgus monkeys by the hot-water tail-withdrawal procedure. TRK-820 given intramuscularly (i.m.) produced a potent antinociceptive effect that was 295- and 495-fold more potent than morphine with the 50°C and 55°C hot-water tests, respectively, and 40-fold more potent than U-50,488H and 1,000-fold more potent than pentazocine in the 50°C hot-water test. The duration of antinociceptive effects of TRK-820 treatment (0.01 and 0.03 mg/kg, i.m.) lasted more than 6 h, which was much longer than those of U-50,488H. The antinociception produced by the higher dose (0.03 mg/kg, i.m.) of TRK-820 was not inhibited by nor-binaltorphimine (3.2 and 10 mg/kg, s.c.) or by naloxone (0.1 mg/kg, s.c.), although the antinociception induced by a lower dose of TRK-820 (0.01 mg/kg, i.m.) was inhibited by nor-binaltorphimine (10 mg/kg, s.c.). The same doses of nor-binaltorphimine and naloxone effectively inhibited the antinociception induced by the higher doses of U-50,488H (1.0 mg/kg, i.m.) and morphine (10 mg/kg, i.m.), respectively. These results indicate that the antinociception induced by TRK-820 is less sensitive to nor-binaltorphimine and suggest that it is mediated by the stimulation of a subtype of κ-opioid receptor different from the κ1-opioid receptor in cynomolgus monkeys.View full abstractDownload PDF (452K) -
Tong Mook Kang, Young Chul Kim, Jae Hoon Sim, Jong Chul Rhee, Sung Joo ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 291-298
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSWe investigated the properties of carbachol (CCh)-activated nonselective cation channels (NSCCCh) at the single channel level in the gastric myocytes of guinea pigs using a magnified whole-cell mode or an outside-out mode. The channel activity (NPo) recorded in a magnified whole-cell mode increased with depolarization (from −120 to −20 mV) and had the half activation potential of −81 mV under the symmetrical 140 mM Cs+ condition. The single channel conductance depended upon the extracellular monovalent cations with the order of Cs+ (35 pS) > Na+ (25 pS) > Li+ (21 pS). The channel activities markedly diminished or disappeared when external Cs+ was replaced with Na+ or N-methyl-D-glucamate (NMDG+). With Cs+ and Na+ as external cations, the channel showed a monotonic increase in NPo with the increased mole fraction of Cs+ over Na+, and it had an intermediate conductance value in solution containing 67% Cs+ with 33% Na+. These data suggested that the extracellular monovalent cations regulate the whole-cell current of NSCCCh by modulating both the open state probability and the unitary conductance, and there is one binding site for the extracellular cations within the pore.View full abstractDownload PDF (361K) -
Shi Chuen-Chao, Liao Jyh-Fei, Chen Chieh-FuSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 299-305
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSThree psychological active principles from the seeds of Peganum harmala L., harmine, harmaline and harmalol, showed vasorelaxant activities in isolated rat thoracic aorta preparations precontracted by phenylephrine or KCl with rank order of relaxation potency of harmine > harmaline > harmalol. The vasorelaxant effects of harmine and harmaline (but not harmalol) were attenuated by endothelium removal or pretreatment with a nitric oxide (NO) synthase Nω-nitro-L-arginine methyl ester. In cultured rat aortic endothelial cells, harmine and harmaline (but not harmalol) increased NO release, which was dependent on the presence of external Ca2+. In endothelium-denuded preparations, pretreatment of harmine, harmaline or harmalol (3 - 30 μM) inhibited phenylephrine-induced contractions in a non-competitive manner. Receptor binding assays indicated that all 3 compounds interacted with cardiac α1-adrenoceptors with comparable affinities (Ki value around 31 - 36 μM), but only harmine weakly interacted with the cardiac 1,4-dihydropyridine binding site of L-type Ca2+ channels (Ki value of 408 μM). Therefore, the present results suggested that the vasorelaxant effects of harmine and harmaline are attributed to their actions on the endothelial cells to release NO and on the vascular smooth muscles to inhibit the contractions induced by the activation of receptor-linked and voltage-dependent Ca2+ channels. The vasorelaxant effect of harmalol was not endothelium-dependent.View full abstractDownload PDF (611K) -
Hiromi Shimizu, Toshio Kumai, Shinichi KobayashiSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 306-312
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSTo identify the mechanism of cyclosporine-induced hypertension, we studied the effect of cyclosporine on the catecholamine synthetic pathway in rats. We administered cyclosporine (10 mg/kg per day, s.c.) for 3 days to 10-week-old male Wistar rats. Systolic blood pressure increased significantly in the cyclosporine-treated group in comparison to that in the control group. Norepinephrine and epinephrine levels in the adrenal medulla and plasma of cyclosporine-treated rats were also significantly higher than levels in the control rats. Moreover, tyrosine hydroxylase (TH) activity and TH mRNA expression in the adrenal medulla of cyclosporine-treated rats were significantly elevated. Administration of the TH inhibitor α-methyl-p-tyrosine (200 mg/kg, b.i.d., s.c.) for 3 days significantly suppressed cyclosporine-induced increases in systolic blood pressure. Phosphorylation of cyclic AMP responsive element-binding protein (CREB) and its binding activity to DNA in the nuclear fraction from the adrenal medulla of cyclosporine-treated rats were much higher than that of the control rats. Calcineurin protein expression of cyclosporine-treated rats was less than that of the control rats. These results suggest that cyclosporine increased blood pressure via activation of the catecholamine synthetic pathway due to the activation of transcription factor CREB.View full abstractDownload PDF (606K) -
Taeko Hata, Eiji Itoh, Yoshinori Funakami, Katsushi Ishida, Shuji Uchi ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 313-321
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSRats exposed to SART (specific alternation of rhythm in temperature) stress, which are ideal animal models for vagotonia-type dysautonomia, show various changes in cardiac and circulatory systems. In this study, attention was directed to cholinergic function in the SART-stressed rat heart and the effects of AF-DX 116, a specific muscarinic M2 antagonist, on blood pressure and heart rate. The results were compared with those obtained for atropine and pirenzepine. In SART-stressed rats, systolic and diastolic blood pressures (SBP and DBP) were lower than in unstressed rats. Oral AF-DX 116 resulted in greater elevation of DBP than SBP in unstressed rats. In stressed rats, greater and more prolonged elevation of SBP than in unstressed rats was noted, particularly at higher doses. A dose-dependent SBP change in stressed rats, caused by intravenous AF-DX 116, was shifted upward in parallel with that in unstressed groups, unlike with oral administration. The positive chronotropic effect of this drug was smaller in stressed rats than in unstressed rats, in contrast to the pressor effect. SART-stressed rats may thus have an enhanced sympathetic tone in the heart, as well as changes in muscarinic M2 receptors at sympathetic nerve endings and at the heart muscle. The effects of AF-DX 116 on blood pressure and heart rate thus may arise from peripheral action and AF-DX 116 may be useful for treating hypotension related to autonomic imbalance of the vagotonia type.View full abstractDownload PDF (574K) -
Itaru Sakai, Shun-ichiro Izumi, Takayo Murano, Shinji Okuwaki, Tsunehi ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 322-326
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSWater extract from commercial English tea has a potent inhibitory activity against human placenta aldose reductase (NADPH oxidoreductase, E.C.1.1.1.21.). Inhibitory activity was separated into five major fractions by one-step chromatography with a C-18 reverse phase column. The most active fraction was further subjected to reverse phase column chromatography. As a result, a well-known flavone-glycoside, isoquercitrin, was isolated as the most potent chemical. The inhibitory character of isoquercitrin for aldose reductase was a mix of uncompetitive and noncompetitive inhibitions, and its IC50 was 1 × 10−6 M. In rat sciatic nerve tissue preparations, sorbitol accumulation in the presence of high concentrations of glucose (30 mM) was inhibited by 38% at 5 × 10−4 M of isoquercitrin. The flavone-glycoside isoquercitrin is the active inhibitor of aldose reductase inhibitor present in English tea. Given the ability of aldose reductase inhibitors to prevent diabetic complications, an epidemiological study of the effect of tea consumption on the pathogenesis and progression of diabetic complications would be interesting.View full abstractDownload PDF (179K)
Short Communications
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Jun Fujishiro, Taiichiro Imanishi, Jun Baba, Kenji KosakaSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 327-330
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSWe examined the effects of two noradrenergic tricyclic antidepressants and two selective serotonin re-uptake inhibitors in the tail suspension test, with a suspension period of 30 min instead of the usual 10 min. Within the first 10 min, desipramine, nortriptyline and fluvoxamine significantly reduced the duration of immobility. Whereas desipramine and nortriptyline were also efficacious in the rest of the test period, fluvoxamine was not. Fluoxetine showed no significant effect throughout the study period. These results suggest that a prolonged tail suspension test results in functional changes in the noradrenergic and serotonergic systems and alters the sensitivity to antidepressants.View full abstractDownload PDF (138K) -
Akira Takahara, Hideki Dohmoto, Ryota Yoshimoto, Atsushi Sugiyama, Kei ...Subject area: Infomation Science
2001 Volume 85 Issue 3 Pages 331-334
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSCardiovascular effects of a new Ca2+ channel blocker AH-1058, 4-(5H-dibenzo[a,d]cyclohepten-5-ylidene)-1-[(E)-3-(3-methoxy-2-nitro)phenyl-2-propenyl]piperidine hydrochloride, were assessed in conscious dogs using a new telemetry system. AH-1058 (0.03, 0.1 and 0.3 mg/kg, i.v.) reduced systolic blood pressure and the maximal upstroke velocity of the left ventricular pressure and increased the heart rate in a dose-dependent manner without affecting the diastolic blood pressure; each of these responses lasted for several hours. These results support the previous knowledge that AH-1058 is a long-lasting cardiodepressive drug. The telemetry system provided important information for predicting favorable clinical effects of AH-1058.View full abstractDownload PDF (210K)
Rapid Communications
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Kenji Onodera, Ko Zushida, Junzo KameiSubject area: Infomation Science
2001 Volume 85 Issue 3 Pages 335-337
Published: 2001
Released on J-STAGE: May 25, 2001
JOURNAL FREE ACCESSThe antinociceptive effect of vitamin K2 (menatetrenone) in diabetic mice was examined using a tail-pressure test. Intraperitoneal injection of menatetrenone (10 - 100 mg/kg) produced a dose-dependent increase in the nociceptive threshold in diabetic mice. There was no significant difference between non-diabetic and diabetic mice in the menatetrenone-induced changes in the nociceptive threshold. The results suggest the therapeutical usefulness of menatetrenone for treating painful diabetic neuropathy and osteoporosis.View full abstractDownload PDF (144K)
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