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Titlebook: Essential Hypertension; Calcium Mechanisms a Kyuzo Aoki Book 1986 Springer-Verlag Tokyo 1986 hypertension.treatment

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书目名称Essential Hypertension
副标题Calcium Mechanisms a
编辑Kyuzo Aoki
视频video
图书封面Titlebook: Essential Hypertension; Calcium Mechanisms a Kyuzo Aoki Book 1986 Springer-Verlag Tokyo 1986 hypertension.treatment
描述This volume contains papers presented at the First International Symposium on Mechanism and Treatment in Essential Hyperten­ sion, which was held on October 23 and 24, 1985 in Nagoya, Japan. The meeting was an official satellite symposium to the meeting of the Fifth International Symposium on Rats with Spon­ taneous Hypertension and Related Studies in Kyoto, October 20-22, 1985. The Nagoya symposium was made possible by offi­ cial grants from the city of Nagoya and Aichi Prefecture and the generous financial support of many companies. The aim of the symposium was to provide a forum for presen­ tation and discussion of recent advances in the area of essential hypertension, particularly with regard to calcium mechanisms in vasoconstriction and vasodilation in arterial vessels and the func­ tion of arterial smooth muscle. The role of calcium ions in the function of arterial smooth muscle has attracted a great deal of attention in the last two decades. The mode of action of calcium ions was revealed at the molecular level. The hypertension model of the spontaneously hypertensive rat has been widely utilized for research into the fundamental mechanisms of genetic hyperten­ sion, stroke,
出版日期Book 1986
关键词hypertension; treatment
版次1
doihttps://doi.org/10.1007/978-4-431-68048-2
isbn_softcover978-4-431-68050-5
isbn_ebook978-4-431-68048-2
copyrightSpringer-Verlag Tokyo 1986
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Actions of Calcium Agonists and Antagonists on Femoral Arteries of Spontaneously Hypertensive Ratsthe data compared with findings in normotensive Wistar-Kyoto rats (WKY). The addition of Bay k 8644 produced a dose-dependent contraction in the SHR femoral artery with a pD. value of 8.55. The maximum contraction induced by this Ca. agonist (1 x 10–..) was comparable with the maximum developed by e
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Altered Vascular Calcium Metabolism As a Possible Cause of Increased Blood Pressure in Essential Hyphere is little information from human studies as to whether such abnormalities play a role in the development of hypertension, but from rat studies the available evidence does not support a direct connection between EC coupling abnormalities and increased blood pressure, although the possibility can
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Calcium-Membrane Interactions in Smooth Muscle in Relation to Hypertensionractionation technique with special reference to the relationship between the alterations of calcium ion handling in vascular smooth muscle and the pathogenesis of spontaneous hypertension in rats. The calcium-membrane interactions include ATP-dependent Ca-transport, Na-dependent Ca-transport (Na-Ca
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Growth Factors and Vascular Smooth Muscle Cells in Spontaneously Hypertensive Ratsth increased synthesis of collagen and noncollagen protein. Cultured VSMCs from rat aorta appear to be a suitable in vitro system to study the mechanism of cellular proliferation of VSMC, because they are completely free from mechanical and neurohumoral influence. Therefore, the present study was de
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Calcium and Calcium Antagonists on Vascular Damage in Spontaneously and Dahl Hypertensive Rats of transmembrane calcium influx by nifedipine prevented the genetically determined hypertension, cardiac hypertrophy, and renal ischaemia in Aoki spontaneously hypertensive rats. In salt-sensitive Dahl rats, nifedipine and its calcium antagonistic dihydropyridine derivatives prevented vascular fibr
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