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人血小板中激活Na+/H+反向转运体的胞质pH设定点的调节:Na+/Ca2+交换、Na(+)-K(+)-2Cl-协同转运和细胞体积的作用

Regulation of the cytosolic pH set point for activation of the Na+/H+ antiport in human platelets: the roles of the Na+/Ca2+ exchange, the Na(+)-K(+)-2Cl- cotransport and cellular volume.

作者信息

Kimura M, Aviv A

机构信息

Hypertension Research Center, University of Medicine and Dentistry of NJ-NJ Medical School, Newark 07103-2714.

出版信息

Pflugers Arch. 1993 Mar;422(6):585-90. doi: 10.1007/BF00374006.

Abstract

To explore further the mechanisms that regulate the Na+/H+ antiport in human platelets, we examined the effect of Na+ pump inhibition by ouabain and K+ removal from the extracellular medium on parameters of this transport system. Treatment with ouabain resulted in increased cytosolic free Ca2+ and Na+, coupled with an alkaline shift in the cytosolic pH set point for the Na+/H+ antiport. Inhibition of the Na+ pump by the removal of K+ from the medium increased the cytosolic Na+ but not the cytosolic Ca2+; yet this treatment also produced a substantial alkaline shift in the cytosolic pH set point for the Na+/H+ antiport. This effect appeared to relate to a decline in cellular volume and it was attenuated by the Na(+)-K(+)-2 Cl- cotransport inhibitor, bumetanide. These findings indicate: (a) a link between the Na+ pump and the Na+/H+ antiport, mediated by the Na+/Ca2+ exchange and the cytosolic free Ca2+, and (b) a link between the Na+/H+ antiport and the Na(+)-K(+)-2Cl- cotransport through cellular volume.

摘要

为了进一步探究调节人血小板中Na⁺/H⁺逆向转运的机制,我们研究了哇巴因抑制Na⁺泵以及从细胞外培养基中去除K⁺对该转运系统参数的影响。用哇巴因处理导致细胞内游离Ca²⁺和Na⁺增加,同时Na⁺/H⁺逆向转运的细胞内pH设定点发生碱化偏移。从培养基中去除K⁺抑制Na⁺泵会增加细胞内Na⁺,但不会增加细胞内Ca²⁺;然而这种处理也会使Na⁺/H⁺逆向转运的细胞内pH设定点发生显著碱化偏移。这种效应似乎与细胞体积减小有关,并且被Na⁺-K⁺-2Cl⁻协同转运抑制剂布美他尼减弱。这些发现表明:(a) Na⁺泵与Na⁺/H⁺逆向转运之间存在联系,由Na⁺/Ca²⁺交换和细胞内游离Ca²⁺介导;(b) Na⁺/H⁺逆向转运与通过细胞体积的Na⁺-K⁺-2Cl⁻协同转运之间存在联系。

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