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在人体血小板中,金雀异黄素可抑制血管加压素对钠氢交换的升高作用。

Vasopressin elevation of Na+/H+ exchange is inhibited by genistein in human blood platelets.

作者信息

Aharonovits O, Zik M, Livne A A, Granot Y

机构信息

Department of Life Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

出版信息

Biochim Biophys Acta. 1992 Dec 9;1112(2):181-6. doi: 10.1016/0005-2736(92)90390-8.

DOI:10.1016/0005-2736(92)90390-8
PMID:1333802
Abstract

The regulation of intracellular Na+ and pHi in human blood platelets is known to be controlled by the function of the Na+/H+ exchanger. The phosphorylation state of the Na+/H+ exchanger which determines the exchanger activity in human blood platelets is regulated by the activities of protein kinases and protein phosphatases. Observations in this study indicate that arginine vasopressin (AVP) that interacts with a V1 receptor, activates the Na+/H+ exchange in human blood platelets through a genistein-inhibited mechanism. The AVP-activated Na+/H+ exchange is probably not regulated by protein kinase C (PKC), since this activation is not inhibited by staurosporine. The multiple ways in which platelet Na+/H+ exchange can be modulated may indicate the critical role played by this exchanger in the homeostasis control of pHi in human blood platelets.

摘要

已知人血小板中细胞内钠离子(Na⁺)和细胞内pH值(pHi)的调节受Na⁺/H⁺交换体功能的控制。决定人血小板中交换体活性的Na⁺/H⁺交换体的磷酸化状态受蛋白激酶和蛋白磷酸酶活性的调节。本研究中的观察结果表明,与V1受体相互作用的精氨酸加压素(AVP)通过一种受染料木黄酮抑制的机制激活人血小板中的Na⁺/H⁺交换。AVP激活的Na⁺/H⁺交换可能不受蛋白激酶C(PKC)调节,因为这种激活不受星形孢菌素抑制。血小板Na⁺/H⁺交换的多种调节方式可能表明该交换体在人血小板pHi的稳态控制中发挥的关键作用。

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Vasopressin elevation of Na+/H+ exchange is inhibited by genistein in human blood platelets.在人体血小板中,金雀异黄素可抑制血管加压素对钠氢交换的升高作用。
Biochim Biophys Acta. 1992 Dec 9;1112(2):181-6. doi: 10.1016/0005-2736(92)90390-8.
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Modulation of Na+/H+ exchange and intracellular pH by protein kinase C and protein phosphatase in blood platelets.蛋白激酶C和蛋白磷酸酶对血小板中Na+/H+交换及细胞内pH的调节作用
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Intracellular-pH dependence of Na-H exchange and acid loading in quiescent and arginine vasopressin-activated mesangial cells.静息和精氨酸血管加压素激活的系膜细胞中钠氢交换及酸负荷的细胞内pH依赖性
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