Sutudy of vascular reactions in response to hemodynamic factors assessed by stretch activation
通过拉伸激活评估血流动力学因素的血管反应研究
基本信息
- 批准号:04671360
- 负责人:
- 金额:$ 1.34万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1992
- 资助国家:日本
- 起止时间:1992 至 1993
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Cerebral and coronary arteries are extremely sensitive to hemodynamic factors, i.e., biomichacal stimule, including blood pressure and blood flow. I have investigated the ca^<2+>-signaling mechanisms of mechanical reception in the cardiovascular system from the following point of view, and as a leader i have promoted the progress of this relatively underdeveloped research field. I have regarded the myogenic contractile reaction of blood vessels in response to stretch of vascular wall or an increase in intraluminal pressure as a kind of cellular/intracellular and Ca^<2+> signaling ; and 3) the cross-bridge property of contractile elements. I could have showed interesting results as follows which will promise the future progress in the research. I have found that membrane fluidity strongly affects the sensitivity of a mechano-receptor site, and an amiloride-sensitive component, a possible stretch-activated channel, may play a role in the genesis of myogenic activity. In addition, the biomechanical stimulus augmented the activity of phospholipase C, production of inositol trisphosphate, and increase in cytosolic Ca^<2+> concentration, which indicates a possible role of GTP-binging proteins coupled with this enxyme in the transformation of mechanical stimulus to cellular signalings. Moreover, myogenic activity is found to be in-between the contraction produced by phorbol esters and high K^+ depolarizing stimulus in the property of cross-bridge cycling. These results suggest that vascular reaction in response to biomechanical stimuli is mediated through a novel mechanisum of cellular signaling.
大脑和冠状动脉对血液动力学因素非常敏感,即生物刺激,包括血压和血流量。我从以下角度研究了心血管系统机械接收的钙信号机制,并作为领导者推动了这一相对不发达的研究领域的进展。我认为血管对血管壁伸展或腔内压力增加的肌性收缩反应是一种细胞/细胞内和钙信号;3)收缩元件的跨桥特性。我本可以展示以下有趣的结果,这将为未来的研究进展提供保证。我发现,膜流动性强烈影响机械感受器部位的敏感性,而阿米洛利敏感成分,可能是牵张激活的通道,可能在肌源性活动的发生中发挥作用。此外,生物力学刺激增加了磷脂酶C的活性,产生了三磷酸肌醇,并增加了胞内Ca~(2+)浓度,这表明与这种酶结合的GTP结合蛋白在机械刺激向细胞信号的转化中可能发挥了作用。此外,还发现佛波酯的收缩和高K~(++)去极化刺激之间的生肌活动具有跨桥循环的特性。这些结果表明,血管对生物力学刺激的反应是通过一种新的细胞信号机制来调节的。
项目成果
期刊论文数量(136)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yoshio Tanaka, Shinzo Hata, Hiromi Ishiro, Kunio Ishii and Koichi Nakayama: "Stretching releases Ca^<2+> from intracellular sites in canine cerebral arteries." Can.J.Physiol.Pharmacol.in press. (1994)
Yoshio Tanaka、Shinzo Hata、Hiromi Ishiro、Kunio Ishii 和 Koichi Nakayama:“拉伸会从犬脑动脉的细胞内位点释放 Ca^<2>。”
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Yoshio Tanaka, Hiromi Ishiro, Tohru Nakayama, Michihiro Saito, Kunio Ishii and Koichi Nakayama.: "Vasoconstrictory characteristics of endothelin-1 and neuropeptide Y in coronary and cerebral arteries and the effects of Ca^<2+> antagonistic vasodilators."
Yoshio Tanaka、Hiromi Ishiro、Tohru Nakayama、Michihiro Saito、Kunio Ishii 和 Koichi Nakayama.:“冠状动脉和脑动脉中内皮素-1 和神经肽 Y 的血管收缩特性以及 Ca^2 拮抗血管扩张剂的作用。”
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Akihiro Oyabe, Ki-ichiro Ueta, Yoshio Tanaka and Koichi Nakayama: "Amiloride-sensitive mechanism of myogenic constriction of rat cerebral arteries induced by increasing intraluminal pressure." in preparation.
Akihiro Oyabe、Ki-ichiro Ueta、Yoshio Tanaka 和 Koichi Nakayama:“腔内压力增加引起大鼠脑动脉肌源性收缩的阿米洛利敏感机制。”
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中山 貢一 福田 義久: "イオンチャネルの薬理 次世代Ca拮抗薬" CLINICAL NEUROSCIENCE. 10. 435-437 (1992)
Koichi Nakayama 和 Yoshihisa Fukuda:“离子通道药理学:下一代 Ca 拮抗剂”临床神经科学。 10. 435-437 (1992)
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Nakayama,K.,Nozawa,Y.and Fukuta,Y.: "Allosteric interaction of semotiadil fumarate,a novel benzothiazine,with 1,4-dihydropyridines,phenylalkylamine,and 1,5-benzothiazepines at the Ca^<2+>-channel antagonist binding sites in canine skeletal muscle membrane
Nakayama, K.、Nozawa, Y. 和 Fukuta, Y.:“富马酸赛替地尔(一种新型苯并噻嗪)与 1,4-二氢吡啶、苯烷基胺和 1,5-苯并硫氮杂卓类药物在 Ca^2 > 通道上的变构相互作用
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NAKAYAMA Koichi其他文献
NAKAYAMA Koichi的其他文献
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{{ truncateString('NAKAYAMA Koichi', 18)}}的其他基金
The bubble-projection three-dimensional display using generation technology of underwater bubbles
利用水下气泡生成技术的气泡投影三维显示
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24650056 - 财政年份:2012
- 资助金额:
$ 1.34万 - 项目类别:
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Construction of a routing optimization algorithm
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21700180 - 财政年份:2009
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$ 1.34万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Development of cell based artificial joint
基于细胞的人工关节的开发
- 批准号:
19791037 - 财政年份:2007
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Molecular mechanisms for regulation of glucose metabolism in skeletal muscle cells by biomechanical stress.
通过生物力学应激调节骨骼肌细胞葡萄糖代谢的分子机制。
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18590064 - 财政年份:2006
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$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Realtime imaging analysis of tyrosine phosphorylation in response to hemodynamic forces
酪氨酸磷酸化响应血流动力学的实时成像分析
- 批准号:
12470528 - 财政年份:2000
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Role of caveolin located in the caveolae, identified as flask-shaped invaginations on the surface of the plasma membrane, involved in the mechanotrasduction of vascular system.
小凹蛋白的作用位于小凹,被确定为质膜表面的烧瓶状内陷,参与血管系统的机械传导。
- 批准号:
10672046 - 财政年份:1998
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Development of the modulator drug specifically targeting biomechanical reaction in the circulatory system and the application for experimental therapeutics.
开发专门针对循环系统生物力学反应的调节药物及其在实验治疗中的应用。
- 批准号:
08557139 - 财政年份:1996
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Specific role of tyrosine kinase in the vascular contraction produced by stretch.
酪氨酸激酶的特异作用是使血管收缩而产生牵拉。
- 批准号:
07672370 - 财政年份:1995
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Coupling mechanism of mechano-sensing and cellular reactivity in the process of stretch activation of vascular tissue.
血管组织拉伸激活过程中机械传感和细胞反应的耦合机制。
- 批准号:
02671005 - 财政年份:1990
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Study of the stimulus-response relationship in a multi-cellular system by use of stretch-induced contractile activation of vascular tissue.
利用拉伸诱导的血管组织收缩激活来研究多细胞系统中的刺激-反应关系。
- 批准号:
63571051 - 财政年份:1988
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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