The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform
Toshifumi Taguchi - One of the best experts on this subject based on the ideXlab platform.
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decreased Depressor Response mediated by calcitonin gene related peptide cgrp containing vasodilator nerves to spinal cord stimulation and levels of cgrp mrna of the dorsal root ganglia in spontaneously hypertensive rats
Hypertension Research, 2000Co-Authors: Hiromu Kawasaki, Yoshitsugu Nuki, Naka Yamaga, Yuji Kurosaki, Toshifumi TaguchiAbstract:The Depressor Response to electrical stimulation of the spinal cord and the level of calcitonin gene-related peptide (CGRP) mRNA in the dorsal root ganglion (DRG) in the spontaneously hypertensive rat (SHR) was compared with the normotensive Wistar Kyoto rat (WKY) and Wistar rat (WR). The animals were pithed by inserting a stainless-steel rod into the spinal cord. Pithed rats were treated with hexamethonium (2 mg/kg/min i.v.) to block autonomic outflow, and mean arterial blood pressure (MBP) was maintained at approximately 100 mmHg with continuous infusion of methoxamine (10 to 15 microg/kg/min i.v.). Electrical stimulation (2 and 4 Hz for 30 s) of the lower thoracic spinal cord (T9-12) via the pithing rod caused a frequency-dependent Depressor Response without a change in heart rate. The Depressor Response to spinal cord stimulation was significantly smaller in SHR than in WKY and WR. Long-term treatment of 8 week-old SHR with captopril (0.1% in drinking water) for 7 weeks restored the reduced Depressor Response to spinal cord stimulation. The level of CGRP mRNA in DRG of SHR was significantly lower than that in WKY. These results suggest that the function of CGRP-containing nerves from the spinal cord decreases in SHR and captopril treatment prevents its reduction.
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effects of dorsal rhizotomy on Depressor Response to spinal cord stimulation mediated by endogenous calcitonin gene related peptide in the pithed rat
Journal of Neurosurgery, 1993Co-Authors: Yoshitsugu Nuki, Toshifumi Taguchi, Hiromu Kawasaki, Koichiro Takasaki, Akihiko WadaAbstract:✓ The effects of acute and chronic dorsal rhizotomy on vasodilation induced by spinal cord stimulation were investigated in the pithed rat in vivo. Pithed rats were treated intravenously with hexamethonium (2 mg/kg/min) to block autonomic outflow, and mean arterial blood pressure was maintained at approximately 100 mm Hg with methoxamine (10 to 15 µg/kg/min). Electrical stimulation (2 or 4 Hz, 10 V, 1 msec) of the lower thoracic spinal cord (T9–12) via the pithing rod caused a frequency-dependent Depressor Response without a change in heart rate. The Depressor Response to spinal cord stimulation was inhibited by the intravenous administration of human calcitonin gene-related peptide (CGRP) [8–37] (60 nmol/kg/min) or tetrodotoxin (100 µg/kg). In the pithed rat with acute or chronic bilateral dorsal root rhizotomy at lower thoracic levels (T8–12), spinal cord stimulation at 2 and 4 Hz caused no Depressor Response. These results suggest that the Depressor Response to spinal cord stimulation is mediated by en...
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endogenous calcitonin gene related peptide mediates nonadrenergic noncholinergic Depressor Response to spinal cord stimulation in the pithed rat
Circulation Research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, Koichiro TakasakiAbstract:The role of endogenous calcitonin gene-related peptide (CGRP) in the nonadrenergic noncholinergic Depressor Response to spinal cord stimulation was studied in the pithed rat in vivo. Pithed rats were given hexamethonium (2 mg/kg per minute i.v.) to block autonomic outflow, and mean blood pressure was artificially maintained at approximately 100 mm Hg with methoxamine (10-15 micrograms/kg per minute i.v.). Electrical stimulation of the spinal cord at the level of the lower thoracic vertebra (T9-12) caused a fall in blood pressure in a frequency-dependent (0.5-10 Hz), voltage-dependent (2.5-50 V), and pulse duration-dependent (0.25-8 msec) manner. The heart rate did not change during the Depressor Response. The Depressor Response was long lasting, and the maximum Response was elicited by stimulation at 4-6 Hz. The neurotoxin tetrodotoxin (100 micrograms/kg i.v.) abolished the Depressor Response to spinal cord stimulation, whereas treatment with propranolol (0.5 mg/kg per minute i.v.), atropine (0.05 mg/kg p...
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Capsaicin-sensitive nonadrenergic and noncholinergic Depressor Response to spinal cord stimulation in the pithed rat.
Brain research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, K TakasakiAbstract:The effects of capsaicin on nonadrenergic, noncholinergic Depressor Responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1-8 Hz)-dependent fall in elevated MBP. The Depressor Response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the Response. Capsaicin treatment abolished the Depressor Response. These results suggest that spinal cord stimulation causes neurogenic vasodilation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.
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capsaicin sensitive noradrenergic and noncholinergic Depressor Response to spinal cord stimulation in the pithed rat
Brain Research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, Koichiro TakasakiAbstract:Abstract The effects of capsaicin on nonadrenergic, noncholinergic Depressor Responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP) was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1–8 Hz)-dependent fall in elevated MBP. The Depressor Response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the Response. Capsaicin treatment abolished the Depressor Response. These results suggest that spinal cord stimulation causes neurogenic vasolidation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.
Koichiro Takasaki - One of the best experts on this subject based on the ideXlab platform.
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effects of dorsal rhizotomy on Depressor Response to spinal cord stimulation mediated by endogenous calcitonin gene related peptide in the pithed rat
Journal of Neurosurgery, 1993Co-Authors: Yoshitsugu Nuki, Toshifumi Taguchi, Hiromu Kawasaki, Koichiro Takasaki, Akihiko WadaAbstract:✓ The effects of acute and chronic dorsal rhizotomy on vasodilation induced by spinal cord stimulation were investigated in the pithed rat in vivo. Pithed rats were treated intravenously with hexamethonium (2 mg/kg/min) to block autonomic outflow, and mean arterial blood pressure was maintained at approximately 100 mm Hg with methoxamine (10 to 15 µg/kg/min). Electrical stimulation (2 or 4 Hz, 10 V, 1 msec) of the lower thoracic spinal cord (T9–12) via the pithing rod caused a frequency-dependent Depressor Response without a change in heart rate. The Depressor Response to spinal cord stimulation was inhibited by the intravenous administration of human calcitonin gene-related peptide (CGRP) [8–37] (60 nmol/kg/min) or tetrodotoxin (100 µg/kg). In the pithed rat with acute or chronic bilateral dorsal root rhizotomy at lower thoracic levels (T8–12), spinal cord stimulation at 2 and 4 Hz caused no Depressor Response. These results suggest that the Depressor Response to spinal cord stimulation is mediated by en...
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endogenous calcitonin gene related peptide mediates nonadrenergic noncholinergic Depressor Response to spinal cord stimulation in the pithed rat
Circulation Research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, Koichiro TakasakiAbstract:The role of endogenous calcitonin gene-related peptide (CGRP) in the nonadrenergic noncholinergic Depressor Response to spinal cord stimulation was studied in the pithed rat in vivo. Pithed rats were given hexamethonium (2 mg/kg per minute i.v.) to block autonomic outflow, and mean blood pressure was artificially maintained at approximately 100 mm Hg with methoxamine (10-15 micrograms/kg per minute i.v.). Electrical stimulation of the spinal cord at the level of the lower thoracic vertebra (T9-12) caused a fall in blood pressure in a frequency-dependent (0.5-10 Hz), voltage-dependent (2.5-50 V), and pulse duration-dependent (0.25-8 msec) manner. The heart rate did not change during the Depressor Response. The Depressor Response was long lasting, and the maximum Response was elicited by stimulation at 4-6 Hz. The neurotoxin tetrodotoxin (100 micrograms/kg i.v.) abolished the Depressor Response to spinal cord stimulation, whereas treatment with propranolol (0.5 mg/kg per minute i.v.), atropine (0.05 mg/kg p...
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capsaicin sensitive noradrenergic and noncholinergic Depressor Response to spinal cord stimulation in the pithed rat
Brain Research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, Koichiro TakasakiAbstract:Abstract The effects of capsaicin on nonadrenergic, noncholinergic Depressor Responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP) was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1–8 Hz)-dependent fall in elevated MBP. The Depressor Response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the Response. Capsaicin treatment abolished the Depressor Response. These results suggest that spinal cord stimulation causes neurogenic vasolidation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.
Hiromu Kawasaki - One of the best experts on this subject based on the ideXlab platform.
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decreased Depressor Response mediated by calcitonin gene related peptide cgrp containing vasodilator nerves to spinal cord stimulation and levels of cgrp mrna of the dorsal root ganglia in spontaneously hypertensive rats
Hypertension Research, 2000Co-Authors: Hiromu Kawasaki, Yoshitsugu Nuki, Naka Yamaga, Yuji Kurosaki, Toshifumi TaguchiAbstract:The Depressor Response to electrical stimulation of the spinal cord and the level of calcitonin gene-related peptide (CGRP) mRNA in the dorsal root ganglion (DRG) in the spontaneously hypertensive rat (SHR) was compared with the normotensive Wistar Kyoto rat (WKY) and Wistar rat (WR). The animals were pithed by inserting a stainless-steel rod into the spinal cord. Pithed rats were treated with hexamethonium (2 mg/kg/min i.v.) to block autonomic outflow, and mean arterial blood pressure (MBP) was maintained at approximately 100 mmHg with continuous infusion of methoxamine (10 to 15 microg/kg/min i.v.). Electrical stimulation (2 and 4 Hz for 30 s) of the lower thoracic spinal cord (T9-12) via the pithing rod caused a frequency-dependent Depressor Response without a change in heart rate. The Depressor Response to spinal cord stimulation was significantly smaller in SHR than in WKY and WR. Long-term treatment of 8 week-old SHR with captopril (0.1% in drinking water) for 7 weeks restored the reduced Depressor Response to spinal cord stimulation. The level of CGRP mRNA in DRG of SHR was significantly lower than that in WKY. These results suggest that the function of CGRP-containing nerves from the spinal cord decreases in SHR and captopril treatment prevents its reduction.
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effects of dorsal rhizotomy on Depressor Response to spinal cord stimulation mediated by endogenous calcitonin gene related peptide in the pithed rat
Journal of Neurosurgery, 1993Co-Authors: Yoshitsugu Nuki, Toshifumi Taguchi, Hiromu Kawasaki, Koichiro Takasaki, Akihiko WadaAbstract:✓ The effects of acute and chronic dorsal rhizotomy on vasodilation induced by spinal cord stimulation were investigated in the pithed rat in vivo. Pithed rats were treated intravenously with hexamethonium (2 mg/kg/min) to block autonomic outflow, and mean arterial blood pressure was maintained at approximately 100 mm Hg with methoxamine (10 to 15 µg/kg/min). Electrical stimulation (2 or 4 Hz, 10 V, 1 msec) of the lower thoracic spinal cord (T9–12) via the pithing rod caused a frequency-dependent Depressor Response without a change in heart rate. The Depressor Response to spinal cord stimulation was inhibited by the intravenous administration of human calcitonin gene-related peptide (CGRP) [8–37] (60 nmol/kg/min) or tetrodotoxin (100 µg/kg). In the pithed rat with acute or chronic bilateral dorsal root rhizotomy at lower thoracic levels (T8–12), spinal cord stimulation at 2 and 4 Hz caused no Depressor Response. These results suggest that the Depressor Response to spinal cord stimulation is mediated by en...
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endogenous calcitonin gene related peptide mediates nonadrenergic noncholinergic Depressor Response to spinal cord stimulation in the pithed rat
Circulation Research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, Koichiro TakasakiAbstract:The role of endogenous calcitonin gene-related peptide (CGRP) in the nonadrenergic noncholinergic Depressor Response to spinal cord stimulation was studied in the pithed rat in vivo. Pithed rats were given hexamethonium (2 mg/kg per minute i.v.) to block autonomic outflow, and mean blood pressure was artificially maintained at approximately 100 mm Hg with methoxamine (10-15 micrograms/kg per minute i.v.). Electrical stimulation of the spinal cord at the level of the lower thoracic vertebra (T9-12) caused a fall in blood pressure in a frequency-dependent (0.5-10 Hz), voltage-dependent (2.5-50 V), and pulse duration-dependent (0.25-8 msec) manner. The heart rate did not change during the Depressor Response. The Depressor Response was long lasting, and the maximum Response was elicited by stimulation at 4-6 Hz. The neurotoxin tetrodotoxin (100 micrograms/kg i.v.) abolished the Depressor Response to spinal cord stimulation, whereas treatment with propranolol (0.5 mg/kg per minute i.v.), atropine (0.05 mg/kg p...
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Capsaicin-sensitive nonadrenergic and noncholinergic Depressor Response to spinal cord stimulation in the pithed rat.
Brain research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, K TakasakiAbstract:The effects of capsaicin on nonadrenergic, noncholinergic Depressor Responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1-8 Hz)-dependent fall in elevated MBP. The Depressor Response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the Response. Capsaicin treatment abolished the Depressor Response. These results suggest that spinal cord stimulation causes neurogenic vasodilation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.
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capsaicin sensitive noradrenergic and noncholinergic Depressor Response to spinal cord stimulation in the pithed rat
Brain Research, 1992Co-Authors: Toshifumi Taguchi, Hiromu Kawasaki, Takuroh Imamura, Koichiro TakasakiAbstract:Abstract The effects of capsaicin on nonadrenergic, noncholinergic Depressor Responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP) was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1–8 Hz)-dependent fall in elevated MBP. The Depressor Response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the Response. Capsaicin treatment abolished the Depressor Response. These results suggest that spinal cord stimulation causes neurogenic vasolidation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.
Yumi Takemoto - One of the best experts on this subject based on the ideXlab platform.
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Short communication Depressor Responses to L-proline microinjected into the rat ventrolateral medulla are mediated by ionotropic excitatory amino acid receptors
2020Co-Authors: Yumi TakemotoAbstract:The essential amino acid L-proline produces a Depressor Response when microinjected into the caudal ventrolateral medulla (CVLM) of anesthetized rats. L-proline may activate some excitatory amino acid (EAA) receptors. The present study tested this hypothesis by investigating the effects of two ionotropic excitatory amino acid receptor antagonists on the Depressor Response to L-proline in the CVLM: the a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor-selective antagonist 6-cyano-7-nitroquinoxaline-2,3dione (CNQX) and the N-methyl-d-aspartate (NMDA) receptor-selective antagonist MK801. Urethane-anesthetized rats received arterial catheters and their ventrolateral medulla surface was exposed. Injections of the antagonists CNQX and MK801 (2 mM, 68 nl in each case) into the CVLM completely blocked Depressor Responses to subsequent administration of AMPA (2 pmol/34 nl) and NMDA (2 pmol/34 nl), respectively. The Depressor Response to L-proline (3.4 nmol/34 nl) was strongly inhibited by prior injection of CNQX (2 mM, 68 nl) and significantly attenuated by prior injection of a high dose (20 mM, 68 nl), but not a low dose (2 mM, 68 nl), of MK801. The results indicate that the Depressor Response to L-proline in the CVLM includes mechanisms of ionotropic excitatory amino acid receptors. D 2005 Elsevier B.V. All rights reserved.
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Depressor Responses to L-proline microinjected into the rat ventrolateral medulla are mediated by ionotropic excitatory amino acid receptors.
Autonomic neuroscience : basic & clinical, 2005Co-Authors: Yumi TakemotoAbstract:The essential amino acid L-proline produces a Depressor Response when microinjected into the caudal ventrolateral medulla (CVLM) of anesthetized rats. L-proline may activate some excitatory amino acid (EAA) receptors. The present study tested this hypothesis by investigating the effects of two ionotropic excitatory amino acid receptor antagonists on the Depressor Response to L-proline in the CVLM: the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor-selective antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the N-methyl-D-aspartate (NMDA) receptor-selective antagonist MK801. Urethane-anesthetized rats received arterial catheters and their ventrolateral medulla surface was exposed. Injections of the antagonists CNQX and MK801 (2 mM, 68 nl in each case) into the CVLM completely blocked Depressor Responses to subsequent administration of AMPA (2 pmol/34 nl) and NMDA (2 pmol/34 nl), respectively. The Depressor Response to L-proline (3.4 nmol/34 nl) was strongly inhibited by prior injection of CNQX (2 mM, 68 nl) and significantly attenuated by prior injection of a high dose (20 mM, 68 nl), but not a low dose (2 mM, 68 nl), of MK801. The results indicate that the Depressor Response to L-proline in the CVLM includes mechanisms of ionotropic excitatory amino acid receptors.
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l proline microinjected into the rat ventrolateral medulla induces a Depressor Response distinct from l glutamate
Japanese Journal of Physiology, 2004Co-Authors: Yumi TakemotoAbstract:The neurotransmitter candidate L-proline elicits changes in the cardiovascular system via actions in the brainstem. However, its action have not yet been determined in the ventrolateral medulla (VLM), a brain region critical in mediating vasomotor sympathetic nervous system Responses. Microinjections of L-glutamate produce Depressor Responses in the caudal (C) VLM, but pressor Responses in the rostral (R) VLM and the caudal pressor area (CPA) in the far caudal CVLM. The present study tested whether microinjections of l-proline in the VLM produce a pattern of hemodynamic Responses distinct from that of l- glutamate. Urethane-anesthetized rats received arterial catheters and were implanted with flow probes around the abdominal aorta (supplies hindquarters). The surface of each rat's VLM was then exposed. L-Proline induced dose- dependent Depressor Responses in the CVLM (0.003–1.0 M, 34 nl), but did not induce hemodynamic Responses in sites of the RVLM (0.01–1.0 M, 34 nl) that responded to L-glutamate (0.01 M, 34 nl). L-Proline injections (0.1 M, 34 nl) induced rapid and consistent Depressor Responses correlated with coincident decreases in hindquarter resistance (arterial blood pressure/flow) in the CVLM and CPA, but only inconsistent Responses in a few sites in the RVLM. In summary, L-proline induced a distinct pattern of Depressor Responses preferentially in caudal regions of the VLM, and these Depressor effects were associated with decreases in hindquarter resistance. These findings indicate that l-proline may have unique roles including cardiovascular regulation independently from L-glutamate, especially in caudal region of the VLM, via a mechanism that involves altering hindquarter resistance.
De Pei Li - One of the best experts on this subject based on the ideXlab platform.
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correction hypobaric intermittent hypoxia attenuates hypoxia induced Depressor Response
PLOS ONE, 2013Co-Authors: Fang Yuan, Ze Fei Dong, Zhao Nian Zhou, David D Kline, Yi Zhang, De Pei LiAbstract:In Figure 6, Panel D, the delta HR (y-axis) number should be as follows: -25, -50, -75, -100.
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hypobaric intermittent hypoxia attenuates hypoxia induced Depressor Response
PLOS ONE, 2012Co-Authors: Fang Yuan, Ze Fei Dong, Zhao Nian Zhou, David D Kline, Yi Zhang, De Pei LiAbstract:Background Hypobaric intermittent hypoxia (HIH) produces many favorable effects in the cardiovascular system such as anti-hypertensive effect. In this study, we showed that HIH significantly attenuated a Depressor Response induced by acute hypoxia.