Cultured rat vascular smooth muscle cells: extracellular calcium and Na+-K+ regulation.

Cultured rat vascular smooth muscle cells: extracellular calcium and Na+-K+ regulation.
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培养的大鼠血管平滑肌细胞:细胞外钙和Na-K调节。

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发表时间:
1985
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通讯作者:
A. Aviv
A. Aviv
中科院分区:
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文献类型:
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作者:
M. Kino;A. Tokushige;H. Tamura;L. Hopp;B. Searle;F. Khalil;A. Aviv

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本研究探讨了细胞外钙(Cao)与Na+-K+调节之间的关系,因为它特别涉及培养的源自Sprague-Dawley大鼠的血管平滑肌细胞(VSMCs)中Na+泵的活性。与在含0.5、2.0或4.0 mM钙的培养基中培养的细胞相比,当钠泵活跃时,在缺钙培养基中培养的VSMCs细胞内钠含量显著增加,而细胞内钾含量无显著变化。随着细胞内钠的增加,钠泵的活性增强。当钠泵被抑制时,在高钙培养基(Cao = 4.0 mM)或缺钙培养基中培养的VSMCs比在含0.5或2.0 mM钙培养基中培养的细胞表现出更大的细胞内钾下降。此外,当钠泵被抑制时,在缺钙培养基中培养的VSMCs比在含钙培养基中培养的VSMCs表现出更高的细胞内钠水平。通量实验表明,上述变化反映了膜对Na+和K+的渗透性增加。综上所述,Cao通过调节VSMC膜的通透性,在胞内Na+-K+稳态中起重要作用,其对Na泵的影响是通过胞内Na+和K+浓度的扰动介导的。
This study explores the relationship between extracellular calcium (Cao) and Na+-K+ regulation as it particularly pertains to the activity of the Na+ pump in cultured vascular smooth muscle cells (VSMCs) originating from Sprague-Dawley rats. As compared with cells incubated in media containing 0.5, 2.0, or 4.0 mM calcium, when the Na pump is active, VSMCs incubated in a Ca-deficient medium show a marked increase in intracellular sodium and no significant change in intracellular potassium. Associated with the rise in intracellular sodium there is an augmented activity of the Na pump. When the Na pump is inhibited, VSMCs incubated in either high-Ca medium (Cao = 4.0 mM) or Ca-deficient medium manifest a greater decline in intracellular potassium than cells incubated in media containing 0.5 or 2.0 mM calcium. Furthermore, when the Na pump is inhibited, VSMCs incubated in a Ca-deficient medium exhibit higher intracellular sodium levels in comparison with their counterparts incubated in media containing calcium. Flux experiments indicate that the aforementioned changes reflect increased membrane permeabilities to Na+ and K+. It is concluded that by regulating the permeability of the VSMC membrane, Cao plays an important role in the intracellular Na+-K+ homeostasis and that its effect on the Na pump is mediated via perturbations in the intracellular Na+ and K+ concentrations.