Depletion of Oestrogen Receptor‐β Expression in Magnocellular Arginine Vasopressin Neurones by Hypovolaemia and Dehydration

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Abstract
Oestrogen receptor (ER)-beta expression correlates inversely with osmotic control of arginine vasopressin (AVP) release such that cellular dehydration induced by 72 h of 2% saline consumption depletes ER-beta in the magnocellular AVP neurones in the supraoptic (SON) and paraventricular nuclei (PVN). The current studies were performed to determine whether other pathways that stimulate AVP release, such as hypovolaemia, also regulate ER-beta expression in these nuclei, and to evaluate the time course of the change in ER-beta expression during water deprivation and subsequent rehydration. ER-beta expression was evaluated immunocytochemically. In rats made hypovolaemic with a subcutaneous injection of 40% polyethylene glycol (PEG), a significant depletion of ER-beta in both SON and magnocellular PVN (P </= 0.001) was evident 8 h post PEG injection. ER-beta was also significantly depleted following 20 h and 26 h of water deprivation in SON (P = 0.003) and magnocellular PVN (P < 0.001). Six hours of rehydration in rats that had been water deprived for 26 h induced recovery of expression that was statistically significant, although not complete (P </= 0.015 in PVN). Thus, for the first time, the present studies demonstrate that haemodynamic in addition to osmotic influences are capable of regulating ER-beta expression in the magnocellular system, and that the combination of these factors induced by a physiological manipulation (e.g. 20 h of water deprivation) can eliminate ER-beta expression. Because ER-beta has been shown to mediate inhibition of AVP secretion in explants of the hypothalamic-neurohypophyseal system, these data suggest that down-regulation of ER-beta may contribute to stimulated AVP release during hypovolaemic states such as fluid deprivation and haemorrhage.