Estradiol (E2) decreases fluid intake in the female rat and recent studies from our lab demonstrate that the effect is at least in part mediated by membrane-associated estrogen receptors. Because multiple estrogen receptor subtypes can localize to the cell membrane, it is unclear which receptor(s) is generating the anti-dipsogenic effect of E2. The G protein-coupled estrogen receptor 1 (GPER-1) is a particularly interesting possibility because it has been shown to regulate blood pressure; many drinking-regulatory systems play overlapping roles in the control of blood pressure. Accordingly, we tested the hypothesis that activation of GPER-1 is sufficient to decrease fluid intake in female rats. In support of this hypothesis we found that treatment with the selective GPER-1 agonist G1 reduced AngII-stimulated fluid intake in OVX rats. Given the close association between food and fluid intakes in rats, and previous reports suggesting GPER-1 plays a role in energy homeostasis, we tested the hypothesis that the effect of GPER-1 on fluid intake was caused by a more direct effect on food intake. We found, however, that G1-treatment did not influence short-term or overnight food intake in OVX rats. Together these results reveal a novel effect of GPER-1 in the control of drinking behavior and provide an example of the divergence in the controls of fluid and food intakes in female rats.
Keywords: Angiotensin II; Estradiol; Estrogen; Estrogen receptor; Food intake; GPR30.
Copyright © 2015 Elsevier Inc. All rights reserved.