Chronic kidney disease (CKD) patients have exercise intolerance associated with increased cardiovascular mortality. Previous studies demonstrate that blood pressure (BP) and sympathetic nerve responses to handgrip exercise are exaggerated in CKD. These patients also have decreased nitric oxide (NO) bioavailability and endothelial dysfunction which could potentially lead to an impaired ability to vasodilate during exercise. We hypothesized that CKD patients have exaggerated BP responses during maximal whole body exercise and that endothelial dysfunction correlates with greater exercise pressor responses in these patients. Brachial artery flow-mediated dilation (FMD) was assessed before maximal treadmill exercise in 56 participants: 38 CKD (56.7±1.2 years old, 38 males) and 21 controls (52.8±1.8 years old, 20 males). During maximal treadmill exercise, the slope-of-rise in systolic BP (+10.32 mmHg/stage vs. +7.75 mmHg/stage, p<0.001), mean arterial pressure (+3.50 mmHg/stage vs. +2.63 mmHg/stage, p=0.004), and heart rate (+11.87 mmHg/stage vs. +10.69 mmHg/stage, p=0.031) was significantly greater in CKD compared to controls. Baseline FMD was significantly lower in CKD (2.76±0.42% vs. 5.84±0.97%, p=0.008). Lower FMD values were significantly associated with a higher slope of rise in systolic BP (+11.05 mmHg/stage vs. 8.71 mmHg/stage, p=0.003) during exercise in CKD, as well as poorer exercise capacity measured as peak oxygen uptake (VO2 peak; 19.47±1.47 ml min-1 kg-1 vs. 24.57±1.51 ml min-1 kg1, p<0.001). These findings demonstrate that low FMD in CKD correlates with augmented BP responses during exercise and lower peak VO2, suggesting that endothelial dysfunction may contribute to exaggerated exercise pressor responses and poor exercise capacity in CKD patients.