The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform
Michiaki Takato - One of the best experts on this subject based on the ideXlab platform.
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an activation of synaptosomal na k atpase by a novel Dibenzoxazepine Derivative by 1949 in the rat brain its functional role in the neurotransmitter uptake systems
Journal of Neurochemistry, 1992Co-Authors: Toshiaki Nagafuji, Tohru Koide, Tatsuo Miyauchi, Michiaki TakatoAbstract:In search of factors mitigating the final outcome of ischemic and epileptic brain damage, we tested a novel Dibenzoxazepine Derivative (BY-1949), as the compound has been shown to be effective under these two conditions. First, using rat brain, we assessed whether or not BY-1949 affects the Na+,K(+)-ATPase activity. Although in vitro applications of either BY-1949 or its three major metabolites did not cause any apparent effects, both acute and chronic oral administrations of the compound (10 mg/kg) invariably increased the Na+,K(+)-ATPase activity in the synaptosomal plasma membranes by increasing Vmax values. Second, it was shown by this study that the drug treatment caused marked increases in the uptake of both glutamic acid and gamma-aminobutyric acid into the synaptosomes. These results suggest that the activity against ischemic/epileptic brain damage by BY-1949 is explicable, at least partly, in terms of improvement of ionic derangements across the neural membranes via Na+,K(+)-ATPase activation.
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the role of cgmp in the anti aggregating properties of by 1949 a novel Dibenzoxazepine Derivative
European Journal of Pharmacology, 1991Co-Authors: Junichiro Aono, Tohru Koide, Makoto Sugawa, Michiaki TakatoAbstract:The anti-aggregatory activity of a novel agent, BY-1949, 3-methoxy-11-methyldibenz (b,f) (1,4) oxazepine-8-carboxylic acid, was examined using rabbit platelets. Oral administration of BY-1949 (10 or 30 mg/kg) inhibited platelet aggregation induced by ADP, collagen, and arachidonate in a dose-related fashion. In in vitro studies, however, neither BY-1949 nor its major metabolites inhibited platelet aggregation, even at a concentration similar to that attained in plasma in vivo. With regard to the anti-aggregatory action of BY-1949, biochemical analysis revealed that BY-1949 preferentially augmented cyclic GMP (cGMP) formation, via inhibition of phosphodiesterase activity, without altering cyclic AMP (cAMP) formation. Furthermore, the in vitro anti-aggregatory activity was significantly enhanced when the platelets were concomitantly treated with nitric oxide (NO). Based on these results, it is suggested that the in vivo anti-aggregatory effects of BY-1949 are at least partly elicited via platelet/endothelium interactions, in which cGMP plays a pivotal role.
Tohru Koide - One of the best experts on this subject based on the ideXlab platform.
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an activation of synaptosomal na k atpase by a novel Dibenzoxazepine Derivative by 1949 in the rat brain its functional role in the neurotransmitter uptake systems
Journal of Neurochemistry, 1992Co-Authors: Toshiaki Nagafuji, Tohru Koide, Tatsuo Miyauchi, Michiaki TakatoAbstract:In search of factors mitigating the final outcome of ischemic and epileptic brain damage, we tested a novel Dibenzoxazepine Derivative (BY-1949), as the compound has been shown to be effective under these two conditions. First, using rat brain, we assessed whether or not BY-1949 affects the Na+,K(+)-ATPase activity. Although in vitro applications of either BY-1949 or its three major metabolites did not cause any apparent effects, both acute and chronic oral administrations of the compound (10 mg/kg) invariably increased the Na+,K(+)-ATPase activity in the synaptosomal plasma membranes by increasing Vmax values. Second, it was shown by this study that the drug treatment caused marked increases in the uptake of both glutamic acid and gamma-aminobutyric acid into the synaptosomes. These results suggest that the activity against ischemic/epileptic brain damage by BY-1949 is explicable, at least partly, in terms of improvement of ionic derangements across the neural membranes via Na+,K(+)-ATPase activation.
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the role of cgmp in the anti aggregating properties of by 1949 a novel Dibenzoxazepine Derivative
European Journal of Pharmacology, 1991Co-Authors: Junichiro Aono, Tohru Koide, Makoto Sugawa, Michiaki TakatoAbstract:The anti-aggregatory activity of a novel agent, BY-1949, 3-methoxy-11-methyldibenz (b,f) (1,4) oxazepine-8-carboxylic acid, was examined using rabbit platelets. Oral administration of BY-1949 (10 or 30 mg/kg) inhibited platelet aggregation induced by ADP, collagen, and arachidonate in a dose-related fashion. In in vitro studies, however, neither BY-1949 nor its major metabolites inhibited platelet aggregation, even at a concentration similar to that attained in plasma in vivo. With regard to the anti-aggregatory action of BY-1949, biochemical analysis revealed that BY-1949 preferentially augmented cyclic GMP (cGMP) formation, via inhibition of phosphodiesterase activity, without altering cyclic AMP (cAMP) formation. Furthermore, the in vitro anti-aggregatory activity was significantly enhanced when the platelets were concomitantly treated with nitric oxide (NO). Based on these results, it is suggested that the in vivo anti-aggregatory effects of BY-1949 are at least partly elicited via platelet/endothelium interactions, in which cGMP plays a pivotal role.
Toshiaki Nagafuji - One of the best experts on this subject based on the ideXlab platform.
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an activation of synaptosomal na k atpase by a novel Dibenzoxazepine Derivative by 1949 in the rat brain its functional role in the neurotransmitter uptake systems
Journal of Neurochemistry, 1992Co-Authors: Toshiaki Nagafuji, Tohru Koide, Tatsuo Miyauchi, Michiaki TakatoAbstract:In search of factors mitigating the final outcome of ischemic and epileptic brain damage, we tested a novel Dibenzoxazepine Derivative (BY-1949), as the compound has been shown to be effective under these two conditions. First, using rat brain, we assessed whether or not BY-1949 affects the Na+,K(+)-ATPase activity. Although in vitro applications of either BY-1949 or its three major metabolites did not cause any apparent effects, both acute and chronic oral administrations of the compound (10 mg/kg) invariably increased the Na+,K(+)-ATPase activity in the synaptosomal plasma membranes by increasing Vmax values. Second, it was shown by this study that the drug treatment caused marked increases in the uptake of both glutamic acid and gamma-aminobutyric acid into the synaptosomes. These results suggest that the activity against ischemic/epileptic brain damage by BY-1949 is explicable, at least partly, in terms of improvement of ionic derangements across the neural membranes via Na+,K(+)-ATPase activation.
Tatsuo Miyauchi - One of the best experts on this subject based on the ideXlab platform.
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an activation of synaptosomal na k atpase by a novel Dibenzoxazepine Derivative by 1949 in the rat brain its functional role in the neurotransmitter uptake systems
Journal of Neurochemistry, 1992Co-Authors: Toshiaki Nagafuji, Tohru Koide, Tatsuo Miyauchi, Michiaki TakatoAbstract:In search of factors mitigating the final outcome of ischemic and epileptic brain damage, we tested a novel Dibenzoxazepine Derivative (BY-1949), as the compound has been shown to be effective under these two conditions. First, using rat brain, we assessed whether or not BY-1949 affects the Na+,K(+)-ATPase activity. Although in vitro applications of either BY-1949 or its three major metabolites did not cause any apparent effects, both acute and chronic oral administrations of the compound (10 mg/kg) invariably increased the Na+,K(+)-ATPase activity in the synaptosomal plasma membranes by increasing Vmax values. Second, it was shown by this study that the drug treatment caused marked increases in the uptake of both glutamic acid and gamma-aminobutyric acid into the synaptosomes. These results suggest that the activity against ischemic/epileptic brain damage by BY-1949 is explicable, at least partly, in terms of improvement of ionic derangements across the neural membranes via Na+,K(+)-ATPase activation.
Junichiro Aono - One of the best experts on this subject based on the ideXlab platform.
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the role of cgmp in the anti aggregating properties of by 1949 a novel Dibenzoxazepine Derivative
European Journal of Pharmacology, 1991Co-Authors: Junichiro Aono, Tohru Koide, Makoto Sugawa, Michiaki TakatoAbstract:The anti-aggregatory activity of a novel agent, BY-1949, 3-methoxy-11-methyldibenz (b,f) (1,4) oxazepine-8-carboxylic acid, was examined using rabbit platelets. Oral administration of BY-1949 (10 or 30 mg/kg) inhibited platelet aggregation induced by ADP, collagen, and arachidonate in a dose-related fashion. In in vitro studies, however, neither BY-1949 nor its major metabolites inhibited platelet aggregation, even at a concentration similar to that attained in plasma in vivo. With regard to the anti-aggregatory action of BY-1949, biochemical analysis revealed that BY-1949 preferentially augmented cyclic GMP (cGMP) formation, via inhibition of phosphodiesterase activity, without altering cyclic AMP (cAMP) formation. Furthermore, the in vitro anti-aggregatory activity was significantly enhanced when the platelets were concomitantly treated with nitric oxide (NO). Based on these results, it is suggested that the in vivo anti-aggregatory effects of BY-1949 are at least partly elicited via platelet/endothelium interactions, in which cGMP plays a pivotal role.