Further studies aimed at elucidating the pathophysiologic mechanisms underlying the role of vitamin D hormone 1α,25-dihydroxy vitamin D3 (1,25(OH)2D3) showed VDR-deficient mice exhibited lower bioavailability of nitric oxide (NO) due to reduced endothelial NO synthase expression, resulting in increased endothelial dysfunction, arterial stiffness, aortic impedance and remodeling, and overall impaired systolic and diastolic heart function which was independent of the alterations in (RAS) (55). The gene discussed is VDR; the disease is endothelial dysfunction.