Vascular stiffening due to elastin deficiency is a leading risk for hypertension and chronic kidney disease (CKD). However, the mechanisms by which elastin deficiency is involved in the pathogenesis of hypertension and/or CKD are poorly understood. Here, we used elastin heterozygous mice ( Eln+/- ), an animal model of elastin insufficiency, to test the hypothesis that renal dysfunction due to elastin deficiency occurs independently of and precedes the development of hypertension in this mouse model. We assessed blood pressure (BP) and renal hemodynamics in 30-day (P30) and 12-week old anesthetized male and female mice. At P30, mean blood pressure of Eln+/- was similar to wild type (WT) controls ( Eln+/- , 79 ± 5 vs. WT, 69±3 mmHg, P = 0.06); however, renal blood flow was lower ( Eln+/- 2.9 ± 0.2 vs. WT 4.0 ± 0.5 mL/min/g KW, P = 0.03) whereas renal vascular resistance (RVR; Eln+/- 29 ± 3 vs. WT 18 ± 3 mmHg/mL/min/g KW, P = 0.03) was augmented at baseline in Eln+/- mice. At 12 wks old, RVR remained elevated while filtration fraction was higher in male Eln+/- relative to WT mice ( Eln+/- 44 ± 3 vs. WT 38±5 % P = 0.07). Eln+/- mice showed isolated systolic hypertension that was evident only at nighttime ( Eln+/- 136 ± 2 vs. WT 112 ± 6 mmHg, P <0.01). Acute salt loading with 6% dietary sodium increased daytime systolic blood pressure only in male Eln+/- mice ( Eln+/- 118 ± 5 vs. WT 102 ± 6 mmHg, P = 0.03), causing a rightward shift and blunted slope of the pressure-natriuresis curve. Renal interlobar artery basal tone and myogenic response to increasing intraluminal pressure at P10 were similar ( Eln+/- 78 ± 3 vs. WT 67 ± 6 % P = 0.06) whereas they were augmented at P30 ( Eln+/- 63 ± 4 vs. WT 49 ± 6 % P = 0.05) and at 12 wks old in Eln+/- mice ( Eln+/- 50 ± 2 vs. WT 33 ± 3 % P < 0.01), and normalized by the AT1R blocker, candesartan ( Eln+/- 22 ± 9 vs. WT 8 ± 5 % P = 0.10). We conclude that AT1R mediates augmented mechanotransduction and renal vascular dysfunction due to Eln insufficiency that in turn contribute to altered renal sodium handling and increased BP. Such prolonged systemic BP elevation leads to glomerular structural damage due to high renal perfusion pressure. Therefore, therapies that target the AT1R to control BP in patients with elastin deficiency may be beneficial in preventing hypertension-evoked kidney damage.