Abstract
Cardiovascular diseases are more prevalent in patients with chronic kidney disease than in the general population and they are considered the leading cause of death in patients with end-stage renal disease. The discovery that vitamin D3 plays a considerable role in cardiovascular protection has led, in recent years, to an increase in the administration of therapies based on the use of this molecule; nevertheless, several studies warned that an excess of vitamin D3 may increase the risk of hypercalcemia and vascular calcifications. In this study we evaluated the effects of vitamin D3, and of its selective analog paricalcitol, on immature cardiomyocytes. Results show that vitamin D3 induces cAMP-mediated cell proliferation and significant intracellular calcification. Paricalcitol, however, induces cell differentiation, morphological modifications in cell shape and size, and no intracellular calcification. Furthermore, vitamin D3 and paricalcitol differently affect cardiomyoblasts responses to acetylcholine treatment. In conclusion, our results demonstrate that the effects of vitamin D3 and paricalcitol on cardiomyoblasts are different and, if these in vitro observations could be extrapolated in vivo, they suggest that paricalcitol has the potential for cardiovascular protection without the risk of inducing intracellular calcification.
Highlights
The National Kidney Foundation Task Force on Cardiovascular Disease recommends that chronic kidney disease (CKD) patients be considered among the highest risk group for developing cardiovascular (CV) disease [1]
Data obtained from cell viability assay show that treatment for 48 h with vitamin D3 or paricalcitol induces a similar dose-dependent response
Vitamin D3 and Paricalcitol induce no significant differences in cell viability in comparison to control cells
Summary
The National Kidney Foundation Task Force on Cardiovascular Disease recommends that chronic kidney disease (CKD) patients be considered among the highest risk group for developing cardiovascular (CV) disease [1]. CV disease is more prevalent in patients with CKD than in the general population [2] and it is the leading cause of death in patients with end-stage renal disease [1]. It has been reported that nearly 30% of deaths among patients with CKD are to be attributed to cardiovascular causes [3]. CKD associated hyperparathyroidism and mineral metabolism disorders, such as hyperphosphatemia, have been significantly correlated with vascular and visceral calcifications, and with increased risk of CV disease [4]. In addition to vascular problems, left ventricular hypertrophy, subclinical systolic dysfunction, and diastolic dysfunction have been consistently observed in subjects with CKD [5]. It is conjectured that abnormal diastolic function is an independent predictor of decreased aerobic capacity during the early stages of CKD [6]
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