The present study aimed to investigate the role of angiotensin II (Ang II) on sodium appetite in rats subjected to a normal or a low-sodium diet (1% or > 0.1% NaCl) for 4 days. During sodium restriction, a reduction in water intake, urinary volume and sodium excretion was observed. After a low-sodium diet, we observed decreased plasma protein concentrations and haematocrit associated with a slight reduction in arterial pressure, without any significant changes in heart rate, natraemia, corticotrophin-releasing hormone mRNA expression in the paraventricular nucleus and corticosterone levels. After providing hypertonic saline, there was an increase in saline intake followed by a small increase in water intake, resulting in an enhanced saline intake ratio and the recovery of arterial pressure. Sodium deprivation increased plasma but not brain Ang I and II concentrations. A low-sodium diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Moreover, Ang II type 1a receptor mRNA expression was increased in the subfornical organ and the dorsal raphe nucleus and decreased in the medial preoptic nuclei, without changes in the paraventricular nucleus and the nucleus of solitary tract after a low-sodium diet. Blockade of AT(1) receptors or brain Ang II synthesis led to a reduction in sodium intake after a low-sodium diet. Intracerebroventricular injection of Ang II led to a similar increase in sodium and water intake in the control and low-sodium diet groups. In conclusion, the results of the present study suggest that Ang II is involved in the increased sodium appetite after a low-sodium diet.

-Estrogen receptors are located in important brain areas that integrate cardiovascular and hydroelectrolytic responses, including the subfornical organ (SFO) and supraoptic (SON) and paraventricular (PVN) nuclei. The aim of this study was to evaluate the influence of estradiol on cardiovascular and neuroendocrine changes induced by hemorrhagic shock in ovariectomized rats. Female Wistar rats (220 -280 g) were ovariectomized and treated for 7 days with vehicle or estradiol cypionate (EC, 10 or 40 g/kg, sc). On the 8th day, animals were subjected to hemorrhage (1.5 ml/100 g for 1 min). Hemorrhage induced acute hypotension and bradycardia in the ovariectomized-oil group, but EC treatment inhibited these responses. We observed increases in plasma angiotensin II concentrations and decreases in plasma atrial natriuretic peptide levels after hemorrhage; EC treatment produced no effects on these responses. There were also increases in plasma vasopressin (AVP), oxytocin (OT), and prolactin levels after the induction of hemorrhage in all groups, and these responses were potentiated by EC administration. SFO neurons and parvocellular and magnocellular AVP and OT neurons in the PVN and SON were activated by hemorrhagic shock. EC treatment enhanced the activation of SFO neurons and AVP and OT magnocellular neurons in the PVN and SON and AVP neurons in the medial parvocellular region of the PVN. These results suggest that estradiol modulates the cardiovascular responses induced by hemorrhage, and this effect is likely mediated by an enhancement of AVP and OT neuron activity in the SON and PVN.hemorrhage; female rats; supraoptic nuclei; paraventricular nuclei; arterial pressure; heart rate THE PRECISE REGULATION OF body fluids is essential for the metabolic function of virtually all cells in the body. A variety of mechanisms are activated to maintain plasma osmolality and blood volume within a very narrow range of values (3). For example, hypovolemia and/or hypotension induce vasopressin (AVP) and oxytocin (OT) release from the magnocellular neurons of the supraoptic (SON) and paraventricular (PVN) nuclei in the hypothalamus (3, 56). It is estimated that a decrease of 10 -20% in total blood volume induces the release of AVP in several species. This neurosecretory response is modulated by peripheral baroreceptors in the aortic arch and carotid sinus, cardiopulmonary volume receptors, and angiotensin II (ANG II) (50, 65).The precise role of estrogen in maintaining body fluid homeostasis is not yet fully understood (16). Our group has previously reported that ANG II type 1 (AT 1 ) receptors are involved in the regulation of water and hypertonic saline intake in ovariectomized (OVX) rats during the nocturnal period (37, 38). In addition, several reports have suggested that estrogen has modulatory effects on cardiovascular function, as evidenced by the cardiovascular changes observed in postmenopausal women, OVX rats, and, possibly, females of other species during senescence (12, 46). These effects occur by estrogen's action on the...

17β-Estradiol (E2) has been shown to modulate the renin–angiotensin system in hydromineral and blood pressure homeostasis mainly by attenuating angiotensin II (ANGII) actions. However, the cellular mechanisms of the interaction between E2 and angiotensin II (ANGII) and its physiological role are largely unknown. The present experiments were performed to better understand the interaction between ANGII and E2 in body fluid control in female ovariectomized (OVX) rats. The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. In addition, previous data from our group revealed that the ANGII-induced vasopressin (AVP) secretion requires ERK1/2 signaling. Therefore, taken together, the present observations support a novel concept that distinct intracellular ANGII signaling gives rise to distinct neurohypophyseal hormone release. Furthermore, the results show that E2 attenuates p38 MAPK phosphorylation in response to ANGII but not PKC activity in the hypothalamus and the lamina terminalis, suggesting that E2 modulates ANGII effects through the attenuation of the MAPK pathway. In conclusion, this work contributes to the further understanding of the interaction between E2 and ANGII signaling in hydromineral homeostasis, as well as it contributes to further elucidate the physiological relevance of PKC/p38 MAPK signaling on the fluid intake and neurohypophyseal release induced by ANGII.

Secretion of vasopressin (VP), oxytocin (OT) and atrial natriuretic peptide (ANP) is an essential mechanism for the maintenance of hydromineral homeostasis. Secretion of these hormones is modulated by several circulating factors, including oestradiol. However, it remains unclear how oestradiol exerts this modulation. In the present study we investigated the participation of oestradiol in the secretion of VP, OT and ANP and in activation of vasopressinergic and oxytocinergic neurones of the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus in response to extracellular volume expansion (EVE). For this purpose, ovariectomised (OVX) rats treated for 7 days with vehicle (corn oil, 0.1 ml/rat, OVX+O group) or oestradiol (oestradiol cypionate, 10 μg/kg, OVX+E group) were subjected to either isotonic (0.15 m NaCl, 2 ml/100 g b.w., i.v.) or hypertonic (0.30 m NaCl, 2 ml/100 g b.w., i.v.) EVE. Blood samples were collected for plasma VP, OT and ANP determination. Another group of rats was subjected to cerebral perfusion, and brain sections were processed for c-Fos-VP and c-Fos-OT double-labelling immunohistochemistry. In OVX+O rats, we observed that both isotonic and hypertonic EVE increased plasma OT and ANP concentrations, although no changes were observed in VP secretion. Oestradiol replacement did not alter hormonal secretion in response to isotonic EVE, but it increased VP secretion and potentiated plasma OT and ANP concentrations in response to hypertonic EVE. Immunohistochemical data showed that, in the OVX+O group, hypertonic EVE increased the number of c-Fos-OT and c-Fos-VP double-labelled neurones in the PVN and SON. Oestradiol replacement did not alter neuronal activation in response to isotonic EVE, but it potentiated vasopressinergic and oxytocinergic neuronal activation in the medial magnocellular PVN (PaMM) and SON. Taken together, these results suggest that oestradiol increases the responsiveness of vasopressinergic and oxytocinergic magnocellular neurones in the PVN and SON in response to osmotic stimulation.