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.
|Title of host publication||Biochemistry, Physiology and Diagnostics|
|Number of pages||18|
|State||Published - Jan 1 2018|
- Vascular contraction
- Vascular relaxation
- Vessel wall
- Vitamin D