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Angiotensin II receptor subtype 1a (AT1aR) gene silencing in neurons of the subfornical organ (SFO) prevents increased drinking behavior in bile duct ligated rats
Author(s) -
Walch Joseph D.,
Cunningham J. Thomas
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1103.20
Subject(s) - subfornical organ , medicine , candesartan , endocrinology , angiotensin ii , hyponatremia , renin–angiotensin system , thirst , receptor , vasopressin , chemistry , blood pressure
Bile duct ligation (BDL) causes congestive liver failure that is associated with dilutional hyponatremia due to increased fluid intake and vasopressin release. In BDL rats, angiotensin II receptor subtype 1a (AT1aR) gene and protein expression is increased in the subfornical organ (SFO). This project tested the hypothesis that increased AT1aR expression in the SFO contributes to elevated drinking behavior in BDL rats. Rats were injected with an adeno‐associated viral vector containing GFP and either shRNA against AT1aR or scrambled RNA in the SFO. Two weeks later, BDL or sham surgery was performed. Rats were housed in metabolic chambers for measurement of fluid and food intake and urine output. The rats were anesthetized 28 days after BDL surgery and perfused for immunohistochemical analysis and to verify the placement of the injections. BDL rats injected in the SFO with the control construct showed increased water intake compared sham ligated rats injected with either construct. In BDL rats injected in the SFO with AT1aR shRNA, this increase in water intake was significantly attenuated (RM Two‐way ANOVA followed by SNK post‐hoc, P<0.05, n=7–9 per group). These results indicate that angiotensin receptors in the SFO contribute to increased thirst in BDL rats.