Chan Y L, Chatsudthipong V, Wang T
Department of Physiology and Biophysics, University of Illinois College of Medicine, Chicago 60612.
Prog Clin Biol Res. 1988;258:149-60.
The intracellular mechanism of Ang II action, as supported by the present data, may be summarized by the following: Ang II interacts with its receptors, leading to an increase in cytosolic Ca+2 by mobilization of Ca+2 from intracellular pools. This rise in cytosolic Ca+2 initiates the activation of calmodulin-regulated enzymes. This then leads to inhibition of both JV and JHCO3-.
根据目前的数据，血管紧张素II作用的细胞内机制可总结如下：血管紧张素II与其受体相互作用，通过从细胞内储存库中动员钙离子，导致细胞质钙离子增加。细胞质钙离子的这种升高引发钙调蛋白调节酶的激活。然后这导致肾素（JV）和碳酸氢根离子重吸收（JHCO3-）均受到抑制。
