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自发性高血压大鼠不同组织质膜中钙结合的改变

Calcium binding alteration in plasma membrane from various tissues of spontaneously hypertensive rat.

作者信息

Devynck M A, Pernollet M G, Nunez A M, Meyer P

出版信息

Clin Exp Hypertens (1978). 1981;3(4):797-807. doi: 10.3109/10641968109033703.

DOI:10.3109/10641968109033703
PMID:7297326
Abstract

Calcium binding properties of plasma membrane enriched fractions from various tissues were studied in young spontaneously hypertensive rats (SHR) and their normotensive controls (WKY). In all tissues tested (heart, liver, nerve endings, erythrocytes), high affinity calcium binding sites were characterized. Their KD values were in the range of the cytosolic free calcium concentration : (10(-8)-10(-7)). Whatever the tissue, plasma membrane enriched fraction from SHR exhibited a reduced calcium binding capacity but no significant change in affinity. This decrease which averaged 15-25% was also observed in the presence of the calcium ionophore A23187 and thus does not result from a modified accessibility of calcium to its binding sites. It is suggested that this abnormality may be of genetic origin and is possibly implicated in the pathogenesis of hypertension.

摘要

在年轻的自发性高血压大鼠(SHR)及其血压正常的对照大鼠(WKY)中,研究了来自各种组织的富含质膜的组分的钙结合特性。在所有测试的组织(心脏、肝脏、神经末梢、红细胞)中,均鉴定出高亲和力钙结合位点。它们的解离常数(KD)值处于胞质游离钙浓度范围内:(10^(-8)-10^(-7))。无论何种组织,SHR的富含质膜的组分均表现出钙结合能力降低,但亲和力无显著变化。这种平均降低15%-25%的情况在钙离子载体A23187存在时也可观察到,因此并非由钙与其结合位点的可及性改变所致。提示这种异常可能源于遗传,并且可能与高血压的发病机制有关。

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Calcium binding alteration in plasma membrane from various tissues of spontaneously hypertensive rat.自发性高血压大鼠不同组织质膜中钙结合的改变
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引用本文的文献

1
Calmodulin-dependent Ca2+ transport in erythrocytes of spontaneously hypertensive rats.
Pflugers Arch. 1983 Apr;397(1):54-6. doi: 10.1007/BF00585168.
2
Aggregation, membrane potential, and transport in platelets of spontaneously hypertensive rats.
Pflugers Arch. 1984 Nov;402(3):330-6. doi: 10.1007/BF00585519.
3
Decreased content of integral membrane calcium-binding protein (IMCAL) in tissues of the spontaneously hypertensive rat.自发性高血压大鼠组织中膜整合钙结合蛋白(IMCAL)含量降低。
Proc Natl Acad Sci U S A. 1986 Feb;83(4):1097-100. doi: 10.1073/pnas.83.4.1097.
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Platelet abnormalities and the pathophysiology of essential hypertension.血小板异常与原发性高血压的病理生理学
Experientia. 1988 Feb 15;44(2):94-7. doi: 10.1007/BF01952187.
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Defective phosphoinositide metabolism in primary hypertension.原发性高血压中磷酸肌醇代谢缺陷
Experientia. 1988 Feb 15;44(2):133-7. doi: 10.1007/BF01952196.
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Cellular calcium metabolism in primary hypertension.原发性高血压中的细胞钙代谢
Klin Wochenschr. 1987 Feb 16;65(4):155-60. doi: 10.1007/BF01728224.