Weiss S J, Putney J W
J Pharmacol Exp Ther. 1978 Dec;207(3):669-76.
Two agonists, phenylephrine and angiotensin II, which have been shown to alter K+ permeability in the liver were investigated as to the possible role of Ca++ in the K+ release response (measured as 86Rb efflux) in liver slices. Both phenylephrine and angiotensin II caused transient increases in 86Rb efflux from liver slices. For both agonists, the first in a series of responses was independent of extracellular Ca++, but Ca++ was required to obtain a subsequent response. This dependence on extracellular Ca++ for a second response was not receptor-specific suggesting that activation of either receptor elicited the release of the same cellular pool of Ca++. The cationophore, A-23187, only slightly increased 45Ca++ efflux and was without effect on 86Rb efflux. In contrast to the ionophore, phenylephrine stimulated a precipitous rise in 45Ca++ efflux. It is proposed that the liver may be similar to a number of other tissues in that Ca++ mediates changes in K+ permeability, but that the source is a bound Ca++ store, rather than the extracellular space.
两种已被证明可改变肝脏中钾离子通透性的激动剂，去氧肾上腺素和血管紧张素II，被研究了钙离子在肝脏切片钾离子释放反应（以86铷外流衡量）中可能扮演的角色。去氧肾上腺素和血管紧张素II均导致肝脏切片中86铷外流短暂增加。对于这两种激动剂而言，一系列反应中的首个反应均不依赖细胞外钙离子，但需要钙离子才能引发后续反应。对第二个反应依赖细胞外钙离子这一现象并非受体特异性的，这表明激活任一受体都会引发相同细胞内钙离子池的释放。离子载体A-23187仅轻微增加45钙离子外流，且对86铷外流无影响。与离子载体相反，去氧肾上腺素刺激45钙离子外流急剧上升。有人提出，肝脏可能与许多其他组织类似，即钙离子介导钾离子通透性的变化，但其来源是结合型钙离子储存库，而非细胞外空间。
