1.The present study aimed to evaluate, in male adult rats, the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of the fatty acid amide hydrolase (FAAH) activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE). 2.Pretreatment with AEA significantly reduced the effect induced by hypertonic (H-) EVE on prolactin (PRL), oxytocin (OT), corticosterone, but not on vasopressin (AVP) plasma levels. The administration of URB597 alone significantly reduced PRL, OT, AVP and corticosterone in the H-EVE group. Conversely, no significant changes were induced by URB597 or AEA on basal hormone concentrations. Pretreatment with AM251 potentiated OT but did not change AVP plasma levels in the H-EVE group. 3.H-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 neurones co-localizing c-Fos in the SON, but increased the concentrations of nitrate in the median eminence of animals submitted to H-EVE. 4.The present data suggest that: a) vasopressinergic and oxytocinergic neurones may be differentially affected by AEA; 2) the activation of CB1Rs may restrain the response of the neurohypophyseal system (NHS) to EVE; 3) the HPA, PRL and the NHS may be still sensitive to AEA after EVE, being these effects probably not dependent on AEA metabolization; 4) AEA and NO could interact in vivo as modulators to directly control stress-induced responses. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.

PMID:

 

23875874

 

[PubMed – as supplied by publisher]