Foster R, Rasmussen H
Am J Physiol. 1983 Sep;245(3):E281-7. doi: 10.1152/ajpendo.1983.245.3.E281.
The effects of angiotensin II on efflux of radiocalcium and production of aldosterone from dispersed bovine adrenal glomerulosa cells were studied using a flow-through system. Concentrations of angiotensin II between 1.25 X 10(-10) and 1.25 X 10(-8) M were found to stimulate both radiocalcium efflux and the rate of aldosterone production. The increase in radiocalcium efflux occurred within 1.5-2.5 min after angiotensin addition, reached a peak in 3.0-4.5 min, and then declined to a value slightly greater than control. The initial increase in aldosterone production occurred 3-5 min after the peak of calcium efflux. In cells preloaded with [45Ca] and then perfused for 1 h with a medium containing no calcium, the basal rate of aldosterone production fell to zero. Angiotensin II (1.25 X 10(-8) M) caused no increase in aldosterone secretion rate but still caused an efflux of radiocalcium. Exposure of cells to 5 X 10(-5) M verapamil blocked the effect of 1.25 X 10(-10) M angiotensin on both radiocalcium efflux and aldosterone production, but only partially blocked the effects of 1.25 X 10(-8) M angiotensin. In addition to stimulating calcium uptake into adrenal glomerulosa cells, angiotensin II stimulates the mobilization of calcium from an intracellular pool. The precise location of this pool is not known.
采用流通系统研究了血管紧张素II对分散的牛肾上腺球状带细胞放射性钙外流和醛固酮生成的影响。发现浓度在1.25×10⁻¹⁰至1.25×10⁻⁸M之间的血管紧张素II能刺激放射性钙外流和醛固酮生成速率。添加血管紧张素后1.5 - 2.5分钟内放射性钙外流增加,3.0 - 4.5分钟达到峰值,然后降至略高于对照的值。醛固酮生成的初始增加发生在钙外流峰值后3 - 5分钟。在预先加载[⁴⁵Ca]然后用不含钙的培养基灌注1小时的细胞中,醛固酮生成的基础速率降至零。血管紧张素II(1.25×10⁻⁸M)未引起醛固酮分泌速率增加,但仍导致放射性钙外流。将细胞暴露于5×10⁻⁵M维拉帕米可阻断1.25×10⁻¹⁰M血管紧张素对放射性钙外流和醛固酮生成的影响,但仅部分阻断1.25×10⁻⁸M血管紧张素的作用。除了刺激钙摄取进入肾上腺球状带细胞外,血管紧张素II还刺激钙从细胞内池的动员。这个池的确切位置尚不清楚。