Abstract
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 μl−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 μl−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 μl−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.
Highlights
GPER, a newly identified receptor, was cloned and described in 199721
Considering the importance of aldosterone in the control of sodium balance and the immunohistochemical evidence such GPER-immunoreactive cells in the NTS may participate in the control of sodium intake, in the present study, we analyzed whether aldosterone had a rapid action in the NTS that it increased sodium intake and examined whether this effect of aldosterone, if present, was mediated by GPER through the use of GPER blockers and activators
The present study shows that the sodium intake can be rapidly raised by application of aldosterone into the NTS
Summary
GPER, a newly identified receptor, was cloned and described in 199721. It is widely distributed in many tissues, including the placenta, heart, cancer cells, prostate, lymphoid tissue and blood vessels[22,23]. Many immunohistochemical evidences revealed that GPER-immunoreactive cells were present in the NTS24–26. Considering the importance of aldosterone in the control of sodium balance and the immunohistochemical evidence such GPER-immunoreactive cells in the NTS may participate in the control of sodium intake, in the present study, we analyzed whether aldosterone had a rapid action in the NTS that it increased sodium intake and examined whether this effect of aldosterone, if present, was mediated by GPER through the use of GPER blockers and activators
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