Abstract
Estradiol (E2) inhibits fluid intake in several species, which may help to defend fluid homeostasis by preventing excessive extracellular fluid volume. Although this phenomenon is well established using the rat model, it has only been studied directly in young adults. Because aging influences the neuronal sensitivity to E2 and the fluid intake effects of E2 are mediated in the brain, we tested the hypothesis that aging influences the fluid intake effects of E2 in female rats. To do so, we examined water and NaCl intake in addition to the pressor effect after central angiotensin II treatment in young (3–4 months), middle‐aged (10–12 months), and old (16–18 months) ovariectomized rats treated with estradiol benzoate (EB). As expected, EB treatment reduced water and NaCl intake in young rats. EB treatment, however, did not reduce water intake in old rats, nor did it reduce NaCl intake in middle‐aged or old rats. The ability of EB to reduce blood pressure was, in contrast, observed in all three age groups. Next, we also measured the gene expression of estrogen receptors (ERs) and the angiotensin type 1 receptor (AT1R) in the areas of the brain that control fluid balance. ERβ, G protein estrogen receptor (GPER), and AT1R were reduced in the paraventricular nucleus of the hypothalamus in middle‐aged and old rats, compared to young rats. These results suggest the estrogenic control of fluid intake is modified by age. Older animals lost the fluid intake effects of E2, which correlated with decreased ER and AT1R expression in the hypothalamus.
Highlights
It is well established that estradiol (E2) interacts with the renin–angiotensin system to regulate fluid homeostasis in females
The anti-dipsogenic and anti-natriorexigenic effects of E2 have been well characterized (Santollo & Daniels, 2015b), to our knowledge, this is the first report to directly test the effect of aging on the fluid intake effects of E2
Our results demonstrate that while middle-aged rats retain the anti-dipsogenic effect of E2, it is lost in old rats
Summary
Santollo & Daniels, 2015a; Santollo et al, 2016), which is not modulated by progesterone (Kisley et al, 1999; Spiteri et al, 1980; Thrasher & Fregly, 1977). E2 action dampens both the peripheral and central pressor effects of AngII (Jonklaas & Buggy, 1984; Xue et al, 2007) Together these inhibitory effects of E2 act to prevent excessive fluid volume, reduce blood pressure, and from a translational standpoint likely contribute to lower rates of hypertension in premenopausal women (Reckelhoff, 2001). We focused on central AngII administration to isolate the effect of the central pressor response and because AngII action in the brain stimulates fluid intake. To achieve these goals, we used young, middle-a ged, and old adult female rats to test the hypothesis that aging alters the anti-dipsogenic, anti-natriorexigenic, and anti-p ressor effect of E2 after central AngII-treatment
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