Role of estradiol in thirst, sodium appetite and neuroendocrine responses induced by angiotensin II: Cellular mechanisms

Abstract

The renin-angiotensin system plays an important role in controlling the homeostasis of body fluids, being the angiotensin II (Ang II) its main active hormone. The effects dipsogenic, natriorexigenic and neuroendocrine responses of ANG II are mediated mainly by AT1 receptors. In addition, this system is under the influence of female hormones, especially estrogen, which modulate the effects of ANG II mediated by AT1 receptors. However, the molecular and cellular mechanisms of interaction between estradiol and ANG II have not yet been elucidated in the literature. Moreover, the elucidation of the components of cell signaling cascade of AT1 and estrogen receptors provides important information about the role of estrogen modulating the effects of ANG II related hydromineral balance in physiological and pathophysiological conditions such as dehydration and hypovolemia. In this context, the objective of this study is to investigate the influence of estradiol on cell signaling of the AT1 receptor mediating the effects dipsogenic, natriorexigenic and neuroendocrine responses of ANG II induced by water deprivation, acute sodium depletion and central angiotensinergic stimulation in ovariectomized rats.