“…29 Because vascular calcification is independently associated with hypertension in epidemiological studies and RANKL is essential for calcification, it is important to understand that RANKL is an activator of the renin-angiotensin system. 7,30 However, infusion of angiotensin II (100 ng/kg per minute) in ovariectomized ApoE −/− mice significantly increased the expression of RANKL and calcification in vivo, whereas administration of angiotensin II receptor blocker (olmesartan, 3 mg/kg per day) decreased the calcification and expression of bone markers, 30 which introduce a molecular feedback between endocrinology pathways and vascular calcification in the pathogenesis of hypertension. Cross-talk between the renin-angiotensin II and RANKL system has been suggested to work in a vicious cycle to promote vascular calcification in atherosclerosis.…”