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Background: Dietary high salt (HS) intake has a strong impact on cardiovascular diseases. Here, we investigated the link between HS-aggravated immune responses and the development of hypertensive vascular disease., Methods: ApolipoproteinE-deficient mice were transiently treated with HS (1% NaCl) via drinking water for 2 weeks, followed by a washout period, and subsequent Ang II (angiotensin II) infusion (1000 ng/kg per min for 10 days) to induce abdominal aortic aneurysms/dissections and inflammation., Results: While transient HS intake alone triggered nonpathologic infiltration of activated T cells into the aorta, subsequent Ang II infusion increased mortality and the incidence of abdominal aortic aneurysms/dissections and atherosclerosis compared with hypertensive control mice. There were no differences in blood pressure between both groups. In transient HS-treated hypertensive mice, the aortic injury was associated with increased inflammation, accumulation of neutrophils, monocytes, CD69 + CD4 + T cells, as well as CD4 + and CD8 + memory T cells. Mechanistically, transient HS intake increased expression levels of aortic RORγt as well as splenic CD4 + T H 17 and CD8 + T C 1 T cells in Ang II-treated mice. Isolated aortas of untreated mice were incubated with supernatants of T H 17, T H 1, or T C 1 cells polarized in vitro under HS or normal conditions which revealed that secreted factors of HS-differentiated T H 17 and T C 1 cells, but not T H 1 cells accelerated endothelial dysfunction., Conclusions: Our data suggest that transient HS intake induces a subclinical T-cell-mediated aortic immune response, which is enhanced by Ang II. We propose a 2-hit model, in which HS acts as a predisposing factor to enhance hypertension-induced T H 17 and T C 1 polarization and aortic disease., Competing Interests: None.