Arap1 is an interacting protein of angiotensin II type 1 (AT1) receptors and was shown to facilitate trafficking of AT1 receptors to the cell surface in vitro. Here we assessed the tissue localization and possible regulation of Arap1 in vivo. Arap1 was found in various organs of the mouse with an order of expression of heart>kidney>aorta>adrenal gland[asymp]liver[asymp]testis[asymp]spleen>brain, as determined by quantitative RT-PCR. In the kidney, as one of the major target sites of the RAS, we found a gradient of Arap1 mRNA expression along the cortical-medullary axis, with cortical expression levels exceeding those of the inner medulla by 130%. Arap1 protein in the kidney was localized to the renal vasculature including the glomerular capillaries where it overlapped with AT1 receptor expression. Conversely to AT1 receptors, no Arap1 expression was detected in the renal tubular system. Increased oral salt intake (4% NaCl [w/w], 7d, n=5) upregulated renal Arap1 expression by 47% compared to a standard chow (.6% NaCl [w/w], n=5, p=.01). Similar, AT1 antagonism (losartan, 30 mg/kg/d, 7d), increased Arap1 mRNA expression by 52% compared to controls (n=5 each, p<.01). Conversely, unilateral kidney artery stenosis (2k-1c, 20 hrs, n=5) suppressed Arap1 expression compared to controls by 64% and 62% in the clipped and contralateral kidney, respectively (p<.001 vs. control each). In summary, Arap1 is highly expressed in the renal vasculature; Arap1 expression appeared to be regulated inversely to AT1 receptor activation and thus may constitute a measure for local adaptations of the renal vasculature to changes in circulating Ang II levels.