Preiss R, Banaschak H
Acta Biol Med Ger. 1979;38(1):83-96.
Lowering the extracellular K+ content from 6 to 0.6 mM causes a rise, and elevation from 6 to 8.5 mM a fall of 45Ca++ efflux from the vascular smooth muscle cells of the arteria carotis communis of cattle. In contrast, a level of 17 mM K+ has no influence. Removal of extracellular calcium does not block these effects. 10(-4) M ouabain also induces a rise in Ca++ efflux, additional potassium reduction then being without effect; 10(-9) M ouabain is of no influence. The 45Ca++ efflux kinetics correlates with the activity of the isolated Na,K-ATPase. Tonus increases of the vascular strips by 10(-4) M ouabain and potassium deficiency cannot be blocked by 4 mM lanthanum or removal of extracellular calcium. Unlike sodium, potassium stimulates the active Ca++ binding and the activity of the Ca-ATPase of the microsomal fraction. The ative Ca++ binding of the mitochondria is stimulated by both ions. It is postulated that the activity of the plasma membrane Na,K-pump is able to regulate the tonus of big arteries through alteration of Ca++ storage processes.
将细胞外钾离子含量从6 mM降至0.6 mM会导致牛颈总动脉血管平滑肌细胞的45Ca++外流增加，而从6 mM升高至8.5 mM则会使其外流减少45%。相比之下，17 mM的钾离子水平没有影响。去除细胞外钙不会阻断这些效应。10(-4) M哇巴因也会诱导Ca++外流增加，随后进一步降低钾离子则无效果；10(-9) M哇巴因没有影响。45Ca++外流动力学与分离的钠钾ATP酶的活性相关。10(-4) M哇巴因和钾缺乏导致的血管条张力增加不能被4 mM镧或去除细胞外钙所阻断。与钠不同，钾会刺激微粒体部分的活性钙结合和钙ATP酶的活性。两种离子都会刺激线粒体的活性钙结合。据推测，质膜钠钾泵的活性能够通过改变钙储存过程来调节大动脉的张力。
