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Titlebook: Essential Hypertension 2; Kyuzo Aoki Book 1989 Springer Japan 1989 hypertension

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發(fā)表于 2025-3-21 17:00:48 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Essential Hypertension 2
編輯Kyuzo Aoki
視頻videohttp://file.papertrans.cn/316/315455/315455.mp4
圖書封面Titlebook: Essential Hypertension 2;  Kyuzo Aoki Book 1989 Springer Japan 1989 hypertension
描述The First International Symposium on Mechanism and Treatment in Essential Hypertension was held on October 23 and 24, 1985 in Nagoya. The Second International Symposium, which was held on May 30,31, and June 1, 1988 in Nagoya, was a success thanks to the endeavors of all the participants. These symposiums were made possible by the generous support of the city of Nagoya, Aichi Prefec- ture, and various contributions. Understanding of the mechanisms of gene (major gene, essential) hypertension is impossible unless we comprehend the physiological properties of arterial smooth muscle. Since Langendorff‘s discovery of the role of calcium ions in muscle contraction in 1895, we have made immense progress in our knowledge of the role of the calcium ion in the excitation-contraction coupling of the arterial smooth mus- cle. Investigation of the molecular mechanisms controlling the cellu- lar basis of calcium ion action has been established with the discovery of the calcium binding protein (Ebashi 1963). The participation of the calcium induced calcium mechanism in the contraction of muscle has been directly demonstrated by using chemically skinned smooth muscle fibers (Endo et al. 1977). Me
出版日期Book 1989
關(guān)鍵詞hypertension
版次1
doihttps://doi.org/10.1007/978-4-431-68090-1
isbn_softcover978-4-431-68092-5
isbn_ebook978-4-431-68090-1
copyrightSpringer Japan 1989
The information of publication is updating

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Membrane Potential and Calcium Influx in Vascular Muscle from Spontaneously Hypertensive Ratscle cells. Even in veins of new-born SHR, where blood pressure is normotensive, there is a significant shift towards a preponderance of the L-type, rather than the T-type, calcium channel. Changes in calcium influx in SHR would be expected to result in important changes in vascular muscle cell functions.
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Dimas C. Belisario,Leonardo Di. G. Sigalottiscovered among ten Wistar rats supplied from the Animal Center of Kyoto University. It was thought that the hypertension may be of genetic orign. In order to prove this hypothesis I began breeding the hypertensive male rat with a normotensive female rat to obtain genetically hypertensive rats. Many
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https://doi.org/10.1007/978-3-030-88567-0bit mesenteric arteries by a common mechanism, namely by opening voltage-dependent calcium channels. The effects of noradrenaline and membrane depolarization on calcium channels were examined directly at the single channel level using the patch clamp technique. Membrane depolarization increased calc
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Gianluca Baldassarre,Marco Mirolliproduced by stretch, agonistic stimuli, and high K. in helical strips of canine cerebral artery. Simultaneous measurements of the Ca. signals and tension development were made with a fluorimeter. The autofluorescence, motion artifact, and Ca. buffering action, considered as main disadvantages when f
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