Wang Rui, Fang Dan, Lin Tingting, Liang Wenhui, Qiao Hu
Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, China.
Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, China.
Neurosci Lett. 2023 Apr 23;803:137188. doi: 10.1016/j.neulet.2023.137188. Epub 2023 Mar 13.
Sodium intake effect of aldosterone has attracted much attention. In our recent study, aldosterone can play a nongenomic regulatory role on rapid sodium intake in the NTS (nucleus tractus solitarius) by activating G protein-coupled estrogen receptor (GPER), and it exhibited an obvious time-dependent and concentration-dependent regulation. However, the molecular mechanism how aldosterone regulated sodium intake rapidly, is unclear. To determine the molecular mechanism of rapid sodium intake regulation of aldosterone, rats with a stainless-steel cannula in the NTS were used (n = 6 each subgroup), and were injected different concentrations of aldosterone/G1 (GPER agonist)/G15 (GPER antagonist) at different time points, then detected ERK1/2 protein expression. The results showed that aldosterone/G1 increased the ERK1/2 protein phosphorylation, and presented a time-dependent and concentration-dependent similar to sodium intake; Meanwhile, G15 partially blocked this effect at least. Taken together, we postulate that ERK1/2 protein may influence nongenomic sodium intake regulated by aldosterone at nucleus tractus solitarius level.
醛固酮的钠摄入效应备受关注。在我们最近的研究中，醛固酮可通过激活G蛋白偶联雌激素受体（GPER）对孤束核（NTS）中的快速钠摄入发挥非基因组调节作用，且呈现出明显的时间依赖性和浓度依赖性调节。然而，醛固酮如何快速调节钠摄入的分子机制尚不清楚。为确定醛固酮快速调节钠摄入的分子机制，使用了在NTS植入不锈钢套管的大鼠（每个亚组n = 6），并在不同时间点注射不同浓度的醛固酮/G1（GPER激动剂）/G15（GPER拮抗剂），然后检测ERK1/2蛋白表达。结果显示，醛固酮/G1增加了ERK1/2蛋白磷酸化，且呈现出与钠摄入相似的时间依赖性和浓度依赖性；同时，G15至少部分阻断了这种效应。综上所述，我们推测ERK1/2蛋白可能在孤束核水平影响醛固酮调节的非基因组钠摄入。
