The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H‐EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H‐EVE group. Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA‐pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H‐EVE. The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic–pituitary–adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress‐induced responses.