Angiotensin within the brain is required for the polydipsia and hypertension induced by DOCA‐salt (50 mg s.c. pellet, ad lib. 0.15 M NaCl), though the receptors and nuclei involved are unclear. Male mice homozygous for a floxed allele of the AT1AR gene were administered an adenovirus centrally (ICV) encoding either Cre‐recombinase and eGFP (AdCre; n=7), or eGFP alone (AdGFP; n=4). Measurements were first performed at baseline and after virus injection, and then after three weeks of DOCA‐salt treatment. Before DOCA, AdCre caused trends toward reduced total fluid (AdGFP 3.8±0.3; AdCre 2.7±0.4 mL/day) and total sodium (0.57±0.05; 0.47±0.03 mEq/day) intake, and reduced dipsogenic responses to overnight dehydration (AdGFP 0.09±0.001; AdCre 0.06±0.001 mL/2hr, P<0.01). Then, AdCre significantly attenuated the water (15.7±2.3; 8.2±1.8 mL/day, P<0.05) and sodium (1.6±0.4; 1.1±0.3 mEq/day, P<0.05) intake effects of DOCA. AdCre reduced AT1AR mRNA in the subfornical organ (SFO; 1.0±0.7; 0.4±0.3 fold, P<0.05), without significant effect in the PVN, ARC or cortex. Cre‐mediated recombination of genomic DNA was detected in the SFO after AdCre but not AdGFP. These data highlight involvement of brain AT1AR in hydromineral balance. Ongoing work is aimed at measuring the blood pressure effects of brain AT1AR modulation, and site‐specific targeting of the viral vectors to individual brain nuclei. Supported by the NIH and AHA.