Apfeldorf W J, Rasmussen H
Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut.
Cell Calcium. 1988 Apr;9(2):71-80. doi: 10.1016/0143-4160(88)90026-7.
Angiotensin II (AII) induces an initial rapid but transient rise in [Ca2+]i detected with aequorin in bovine adrenal capsule strips. The rise in [Ca2+]i begins immediately after AII addition, reaches a peak in 30 seconds, and returns to near basal values within 5 minutes. The [Ca2+]i transient is receptor-mediated and its height is dose-dependent. The increase in [Ca2+]i is largely due to the release of Ca2+ from an intracellular pool. The uncorrected peak rise in [Ca2+]i after 1 X 10(-6) M beta-[asp1]-AII stimulation is approximately 3 fold, from 110 nM to 300 nM; the peak rise, corrected for diffusion and nonsynchronous cellular response, is from 110 nM to 1.2 microM. Perifusion of aequorin-loaded strips with beta-[asp1]-AII, an aminopeptidase-resistant analog of AII, allows the simultaneous measurement of [Ca2+]i and aldosterone production rate. Levels of agonist which generate a transient rise in [Ca2+]i also produce a sustained increase in aldosterone production rate, but the two events are temporally separated: the transient rise in [Ca2+]i precedes the increase in aldosterone production rate. However, there is a strong correlation, r = 0.94, between the amplitude of the initial [Ca2+]i transient and the magnitude of the sustained increase in steroid production rate.
血管紧张素II(AII)可使牛肾上腺皮质条带中用水母发光蛋白检测到的细胞内钙离子浓度([Ca2+]i)起初迅速但短暂地升高。[Ca2+]i的升高在添加AII后立即开始,30秒内达到峰值,并在5分钟内恢复到接近基础值。[Ca2+]i的短暂变化是由受体介导的,其幅度呈剂量依赖性。[Ca2+]i的升高主要是由于细胞内钙库释放钙离子所致。在1×10(-6)Mβ-[天冬氨酸1]-AII刺激后,未经校正的[Ca2+]i峰值升高约3倍,从110 nM升至300 nM;校正扩散和非同步细胞反应后的峰值升高则从110 nM升至1.2 μM。用β-[天冬氨酸1]-AII(一种对氨肽酶有抗性的AII类似物)对装载有水母发光蛋白的条带进行灌流,可同时测量[Ca2+]i和醛固酮生成率。能使[Ca2+]i短暂升高的激动剂水平也会使醛固酮生成率持续增加,但这两个事件在时间上是分开的:[Ca2+]i的短暂升高先于醛固酮生成率的增加。然而,初始[Ca2+]i短暂变化的幅度与类固醇生成率持续增加的幅度之间存在很强的相关性,r = 0.94。