Cardiovascular complications are the main cause of death in patients with chronic kidney disease (CKD). Among these complications, calcific arteriosclerosis and myocardial hypertrophy are the main predictors of cardiovascular morbidity and mortality. Epidemiological studies have shown their association with hyperparathyroidism, which has therefore been included among the non-traditional cardiovascular risk factors. Studies in laboratory animals have shown that PTH administration may induce calcific arteriosclerosis and myocardial hypertrophy. The former develops independently of hyperphosphatemia, but its mechanisms remain unknown. The latter is characterized by increased thickness of the myocardial fibers and especially the fibrous interstitium; its development is influenced by protein kinase C activation and the subsequent increase in cytosolic calcium as well as activation of intracellular signaling pathways inducing protein synthesis and proliferation. Different from these findings, in other studies PTH infusion was able to produce vasodilatation and to favor myocardial cell contraction and regeneration. These effects depend on protein kinase A activation. PTH may produce different and sometimes contradictory functional effects in the arteries and myocardium that are probably related to different experimental or clinical conditions. In patients with CKD and hyperparathyroidism, PTH may be considered a uremic toxin exerting its effects mainly by increasing cellular calcium. Thus, hyperparathyroidism is confirmed to be a target for the conservative therapy of CKD.