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There are well over 100,000 Americans on the kidney transplant list with a median wait time of 3.6 years. However, about 17 American die each day waiting for a kidney transplant, with vascular calcification being one of the most common causes [1, 2]. One vessel that is highly susceptible to vascular calcification is the aorta leading to negative cardiovascular outcomes that are secondary to kidney disease [3]. Therefore, understanding the effects that kidney disease has on disrupting the physiology of the vasculature, and finding potential therapeutic options, are imperative to those waiting for a life-saving kidney transplant. The present study aimed to test two hypotheses: (1) Aortic calcification leads to a decrease in stress in the thoracic and abdominal aorta of a young adult mouse. (2) The attenuated aortic stress seen in aortic calcification is due to the decreased expression of smooth muscle ⍺-actin (SM⍺-Actin). To test these hypotheses, calcification was induced in the ex vivo mouse aorta, followed by histological staining for calcium deposits, immunoblots for SM⍺-Actin, and measurements of aortic stress. The results of this study support the hypotheses in that calcification impairs aortic stress and it does so by decreasing the expression of SM⍺-Actin. The present study is the first to show the effect of phosphate-induced calcification on stress and expression of SM⍺-Actin in an ex vivo mouse aorta. This study is relevant to researchers as it shows key differences between studying vascular calcification in vitro compared to ex vivo. Therefore, investigating the mechanisms of aortic calcification using an ex vivo model, may be more applicable to human patients.