Vitamin D has recently been shown not only to be important for bone and calcium metabolism but also for homeostasis of critical tissues involved in vascular disease. The vitamin D receptor (VDR) and the 1?-hydroxylase enzyme are present in critical cells implicated in the development of vascular disease. Vitamin D influences multiple mechanisms to decrease vascular inflammation; it suppresses the renin-angiotensin system, promotes endothelial nitric oxide release, decreases vascular inflammatory markers and cholesterol deposition, and imbues immune cells with antiinflammatory properties. Studies in mouse models of diet-induced insulin resistance show that vitamin D deficiency or VDR deletion promotes renin-dependent hypertension and accelerates atherosclerosis. However, the effects of vitamin D supplementation on blood pressure and atherosclerosis have been mixed and depend on baseline vitamin D status, dose and vitamin D compound administered, and animal model. Human observational studies indicate consistent associations between low 25(OH)D levels and increased cardiovascular disease, but the effects of vitamin D supplementation for prevention are conflicting and study design limitations preclude adequate conclusions.

Original languageEnglish
Title of host publicationBiochemistry, Physiology and Diagnostics
PublisherElsevier Inc.
Number of pages18
ISBN (Electronic)9780128099667
ISBN (Print)9780128099650
StatePublished - 2018


  • Angiogenesis
  • Atherosclerosis
  • Hypertension
  • Inflammation
  • Vascular contraction
  • Vascular relaxation
  • Vessel wall
  • Vitamin D


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