Vitamin D and the Cardiovascular System

Vitamin D: beyond bone

“…David G. Gardner (University of California, San Francisco) expanded the discussion of nonclassical effects of vitamin D to include evidence of a significant role for vitamin D in the cardiovascular system. While the heart and vasculature have only recently been identified as potential targets of vitamin D action, a growing body of evidence suggests that the activated VDR plays an important role in regulating cardiovascular function . First, the VDR and the ligand‐generating 25‐hydroxyvitamin D 3 1‐α‐hydroxylase have been shown to be present in cardiac myocytes, cardiac fibroblasts, vascular smooth muscle cells, and vascular endothelial cells.…”

“…While the heart and vasculature have only recently been identified as potential targets of vitamin D action, a growing body of evidence suggests that the activated VDR plays an important role in regulating cardiovascular function. 8 First, the VDR and the ligand-generating 25-hydroxyvitamin D 3 1-␣-hydroxylase have been shown to be present in cardiac myocytes, cardiac fibroblasts, vascular smooth muscle cells, and vascular endothelial cells. Second, vitamin D deficiency in rodents has been shown to elicit increases in blood pressure and cardiac hypertrophy.…”

Low Serum Vitamin D Is Independently Associated with Larger Lesion Volumes after Ischemic Stroke

“…[5][6][7] Potential mechanisms of action include inhibition of thrombogenic influences, 2 attenuation of vascular risk factors, 8 and mitigation of endothelial dysfunction. 2 Accordingly, low vitamin D status may increase cerebral ischemic susceptibility and predilection for larger infarcts. Nevertheless, it is unclear whether vitamin D is independently associated with the infarct volume.…”

“…2 Specifically, low serum 25-hydroxyvitamin D (25[OH] D) has been associated with an increased risk for incident stroke 3,4 and stroke fatality. [5][6][7] Potential mechanisms of action include inhibition of thrombogenic influences, 2 attenuation of vascular risk factors, 8 and mitigation of endothelial dysfunction.…”

Late-onset hypogonadism

“…Less than 1% of testosterone is produced in cells of the adrenal cortex, and less than 5% comes from the peripheral metabolism of its precursors [11, 12]. The substrate for testosterone production is cholesterol, synthesised de novo in Leydig cells or derived from plasma lipoproteins [13]. …”