To address the relative contribution of central and peripheral angiotensin II (ANG II) type 1A receptors (AT_1A) to blood pressure and volume homeostasis, we generated a transgenic mouse model (NSE-AT_1A) with brain-restricted over-expression of AT_1A receptors. These mice are normotensive at baseline but have dramatically enhanced pressor and bradycardic responses to intracerebroventricular (ICV) ANG II or activation of endogenous ANG II production. Here our goal was to examine the water and sodium intake in this model under basal conditions and in response to increased ANG II levels. Baseline water and NaCl (0.3 M) intakes were significantly elevated in NSE-AT_1A compared to non-transgenic littermates, and bolus ICV injections of ANG II (200 ng in 200 nL) caused further enhanced water intake in NSE-AT_1A. Activation of endogenous ANG II production by sodium depletion (10 days low sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT_1A mice compared to wildtypes. Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the AV3V region of the brain in NSE-AT_1A mice compared to control animals. The results show that brain-selective over-expression of AT_1A receptors results in enhanced salt appetite and altered water intake. This model provides a new tool for studying the mechanisms of brain AT_1A -dependent water and salt consumption.