Secondary hyperparathyroidism plays an important role in the mineral and bone disorders that are associated with cardiovascular events in chronic kidney disease patients. Secondary hyperparathyroidism is partially due to decreased calcium-sensing receptor expression in parathyroid glands in these patients. Calcimimetics have been demonstrated to be particularly useful to control parathyroid hormone (PTH) oversecretion and concomitantly reduce serum Ca2+ and phosphorus levels in dialysis patients. However, recent findings highlight the role of calcium-sensing receptor allosteric coactivators as inhibitors of the development of vascular calcification. Calcimimetics could prevent the vascular calcification process by controlling not only PTH overfunction, hypercalcemia and hyperphosphatemia, but also by directly modulating vascular calcium-sensing receptors. In this review, the authors describe the recently demonstrated role played by calcium-sensing receptor and its modulation by calcimimetics on uremia-induced vascular calcification.