Aldosterone induces rapid sodium intake by a nongenomic mechanism in the nucleus tractus solitarius

作者：Qiao, Hu; Hu, Bo; Zhou, Hong; Yan, Jianqun^*; Jia, Ru; Lu, Bo; Sun, Bo; Luo, Xiao; Fan, Yuanyuan; Wang, Nan

来源：Scientific Reports, 2016, 6(1): 38631.

DOI：10.1038/srep38631

• COUPLED ESTROGEN-RECEPTOR
• CENTRAL-NERVOUS-SYSTEM
• PROXIMAL S3 SEGMENT
• MINERALOCORTICOID-RECEPTOR
• SENSITIVE NEURONS
• ENDOTHELIAL-CELLS
• APPETITE
• THIRST
• BRAIN
• RAT

The purpose of this study was to determine whether aldosterone has a rapid action in the nucleus tractus solitarius (NTS) that increases sodium intake, and to examine whether this effect of aldosterone, if present, is mediated by G protein-coupled estrogen receptor (GPER). Adult male Sprague-Dawley rats with a stainless-steel cannula in the NTS were used. Aldosterone was injected into the NTS at the doses of 1, 5, 10 and 20 ng 0.1 mu l(-1). A rapid dose-related increase of 0.3 M NaCl intake was induced within 30 min and this increase was not suppressed by the mineralocorticoid receptor (MR) antagonist spironolactone (10 ng 0.1 mu l(-1)). Water intake was not affected by aldosterone. The GPER agonist G-1 produced a parallel and significant increase in sodium intake, while pre-treatment with GPER antagonist G15 (10 ng 0.1 mu l(-1)) blocked the G-1 or aldosterone-induced rapid sodium intake. In addition, sodium intake induced by sodium depletion or low-sodium diet fell within 30 min after injection into the NTS of the MR antagonist spironolactone, while G15 had no effect. Our results confirm previous reports, and support the hypothesis that aldosterone evokes rapid sodium intake through a non-genomic mechanism involving GPER in NTS.

• 出版日期2016-12-9
• 单位西安交通大学