Lobo M V, Marusic E T
Department of Physiology and Biophysics, Faculty of Medicine, University of Chile, Santiago.
Am J Physiol. 1988 Feb;254(2 Pt 1):E144-9. doi: 10.1152/ajpendo.1988.254.2.E144.
In previous studies it was shown that angiotensin II causes a Ca-dependent increase in the K permeability of bovine adrenal glomerulosa cells [Am. J. Physiol. 250 (Endocrinol. Metab. 13): E125-E130, 1986]. Here we show that angiotensin II causes a significant and prolonged reduction in the 86Rb release immediately after the transient rise in 86Rb efflux. This inhibition was dose related. Apamin (100 nM) and tetraethylammonium (10 mM) completely abolished the initial transient rise in 86Rb efflux without affecting the latter sustained phase of reduced radioisotope release. On the contrary, the effect of angiotensin II on the second phase was absent when Ca was removed from the perifusion medium or replaced with Sr, but the effect on the early transient phase of 86Rb efflux was maintained in the absence of external Ca. An additional finding was the increased coefficient rate of 86Rb efflux that occurred when the cells were depolarized with 12 mM K. However, this effect was not observed when the inhibitory phase due to angiotensin II was fully developed and Ca was present in the external media. On the other hand, the biphasic effect of angiotensin II was still present in depolarized cells. These results suggest that angiotensin II may modulate membrane potential by changes in K permeability of the bovine adrenal glomerulosa cells.
在先前的研究中已表明，血管紧张素II可使牛肾上腺球状带细胞的钾通透性出现钙依赖性增加[《美国生理学杂志》250(内分泌与代谢13):E125 - E130, 1986]。在此我们表明，血管紧张素II在86Rb外流短暂升高后，可使86Rb释放显著且持续减少。这种抑制呈剂量相关。蜂毒明肽(100 nM)和四乙铵(10 mM)完全消除了86Rb外流最初的短暂升高，而不影响随后放射性同位素释放减少的持续阶段。相反，当从灌流培养基中去除钙或用锶替代时，血管紧张素II对第二阶段的作用消失，但在无细胞外钙的情况下，对86Rb外流早期短暂阶段的作用仍存在。另一个发现是，当细胞用12 mM钾去极化时，86Rb外流的系数速率增加。然而，当血管紧张素II引起的抑制阶段充分发展且细胞外培养基中存在钙时，未观察到这种作用。另一方面，血管紧张素II的双相作用在去极化细胞中仍然存在。这些结果表明，血管紧张素II可能通过改变牛肾上腺球状带细胞的钾通透性来调节膜电位。
