**4. Conclusions**

Estradiol replacement therapy initiated at the time of or prior to menopause is usually employed for decreasing the risk of cardiovascular and neurodegenerative diseases [91–93]. Nowadays, the high composition of salt in the contemporary diet constitutes an important public health concern, since uncontrolled sodium consumption increases the risk of hypertension [24], particularly in women in later menopause, who have a greater risk of developing cardiovascular disease [3, 24]. The increased central and peripheral RAS activity is involved in the pathophysiology of hypertension. Given the wide complexity of the crosstalk signaling pathways, cellular and molecular studies are important to better elucidate the mechanisms of the interaction between E2 and ANGII signaling as well as mapping out the potential benefits of E2 replacement and its action on the central nervous system. In this context, advanced evidence has been contributed to the further understanding of E2 and ANGII interaction in the hydromineral homeostasis, which can reveal potential pharmacological targets to prevent cardiovascular diseases, with uncontrolled salt consumption as a predisposing factor, during female reproductive senescence. Taken together, E2 impairs ANGII signaling besides induces the downregulation of AT1 receptor. E2 attenuates MAPKs phosphorylation involved in ANGII physiological actions in the lamina terminalis structures and hypothalamic nuclei, namely, PVN and SON.
