Medical Faculty, Institute of Physiology II, University of Münster, 48149 Münster, Germany.
Kidney Int. 2010 Mar;77(6):490-4. doi: 10.1038/ki.2009.490. Epub 2010 Jan 6.
Dietary sodium and potassium contribute to the control of the blood pressure. Endothelial cells are targets for aldosterone, which activates the apically located epithelial sodium channels. The activity of these channels is negatively correlated with the release of nitric oxide (NO) and determines endothelial function. A mediating factor between channel activity and NO release is the mechanical stiffness of the cell's plasma membrane, including the submembranous actin network (the cell's 'shell'). Changes in plasma sodium and potassium, within the physiological range, regulate the viscosity of this shell and thus control the shear-stress-dependent activity of the endothelial NO synthase located in the shell's 'pockets' (caveolae). High plasma sodium gelates the shell of the endothelial cell, whereas the shell is fluidized by high potassium. Accordingly, this concept envisages that communications between extracellular ions and intracellular enzymes occur at the plasma membrane barrier, whereas 90% of the total cell mass remains uninvolved in these changes. Endothelial cells are highly sensitive to extracellular sodium and potassium. This sensitivity may serve as a physiological feedback mechanism to regulate local blood flow. It may also have pathophysiological relevance when sodium/potassium homeostasis is disturbed.
饮食中的钠和钾有助于控制血压。醛固酮作用于内皮细胞，激活位于顶端的上皮钠通道。这些通道的活性与一氧化氮（NO）的释放呈负相关，并决定了内皮功能。通道活性和 NO 释放之间的中介因素是细胞膜的机械刚性，包括细胞下的肌动蛋白网络（细胞的“壳”）。在生理范围内，血浆中钠和钾的变化调节该壳的粘度，从而控制位于壳“小窝”（ caveolae ）中的内皮型一氧化氮合酶的剪切应力依赖性活性。高血浆钠使内皮细胞的壳凝胶化，而高钾则使壳流化。因此，这一概念设想细胞外离子和细胞内酶之间的通讯发生在质膜屏障处，而 90%的细胞总质量未参与这些变化。内皮细胞对细胞外的钠和钾非常敏感。这种敏感性可能作为一种生理反馈机制，以调节局部血流。当钠/钾稳态受到干扰时，这种敏感性也可能具有病理生理相关性。
