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Effect of Vitamin D on the Treatment and Prevention of Essential Hypertension

Songcang Chen

The vast majority of epidemiological studies have consistently shown that vitamin D levels are inversely related to blood pressure (BP) and the incidence of hypertension (HTN). Animal studies from diet-induced or genetic models of vitamin D deficiency suggest that vitamin D deficiency directly causes HTN. Based on basic and clinical studies, modestly increased renin expression in genetic mouse models of vitamin D deficiency is associated with, but not causally linked to vitamin D deficiency-induced HTN. Our mechanistic studies indicate that overexpression of a novel target gene seems to play a critical role in vitamin D-deficient HTN, and that vitamin D signaling defect in vascular smooth muscle cells and CD4+ T lymphocytes seems predominantly be responsible for vitamin D deficiencymediated HTN. The data from many clinical trials have consistently demonstrated a minimal or no effect of shortterm vitamin D supplementation on BP in normotensive healthy individuals, but long-term vitamin D supplementation should prevent the development of essential HTN (EH) at high-risk susceptible people. More than 13 randomized controlled trials have shown that vitamin D repletion significantly reduces BP in vitamin D-deficient EH patients, which appears to be more effective in those with type 2 diabetes or impaired glucose tolerance. Short-term administration of active vitamin D or its analogue has a better antihypertensive role than natural vitamin D in the treatment of vitamin D-deficient EH. While these promising data from relatively small trials have displayed potential beneficial vitamin D effect on EH, it is urgently needed to comprehensively elucidate molecular mechanisms of vitamin D deficiency-induced HTN, which will provide a solid theoretical basis to well design large randomized controlled trials to further address the antihypertensive role of vitamin D in vitamin D-deficient EH patients. Currently, EH is lacking an etiology-specific therapy. Identification of vitamin D deficiency as an environmental stressor that triggers the development of EH at vulnerable individuals will make a great advance in the field of EH research.