title: Vitamin D, arterial hypertension & cerebrovascular disease.
abstract: Vitamin D is mainly derived from endogenous ultraviolet-B induced vitamin D synthesis in the skin, and the current high prevalence of vitamin D deficiency can, therefore, largely be attributed to lifestyle related low sunlight exposure. Regulation of bone and mineral metabolism is a classic vitamin D effect, but the identification of the vitamin D receptor (VDR) in almost all human cells suggests a role for vitamin D also in extra-skeletal diseases. Experimental studies demonstrated several antihypertensive and vascular protective effects of vitamin D, such as suppression of the renin angiotensin aldosterone system, beneficial modulation of classic cardiovascular risk factors, and anti-atherosclerotic properties including improvements of endothelial function. Additional neuroprotective actions of vitamin D have also been reported. In line with this, epidemiological studies have largely shown that vitamin D deficiency is an independent risk factor for arterial hypertension and strokes. Data from randomized controlled trials (RCTs) are, however, limited and less promising, with currently no confirmation that vitamin D reduces stroke incidence. Whereas some RCTs suggest that vitamin D supplementation might modestly reduce blood pressure, this has not been consistently observed in all studies. It is, therefore, premature to recommend vitamin D supplementation for the prevention and treatment of arterial hypertension and stroke. Nevertheless, the fact that patients with arterial hypertension and cerebrovascular disease are at a relatively high risk of vitamin D deficiency, and therewith associated musculoskeletal diseases can serve as a rationale for the evaluation, prevention and treatment of vitamin D deficiency in these patients.
authors.affiliation: Department of Internal Medicine, Division of Endocrinology & Metabolism, Medical University of Graz, Austria.
authors.forename: Katharina
authors.initials: K
authors.lastname: Kienreich
authors.forename: Martin
authors.initials: M
authors.lastname: Grubler
authors.forename: Andreas
authors.initials: A
authors.lastname: Tomaschitz
authors.forename: Johannes
authors.initials: J
authors.lastname: Schmid
authors.forename: Nicolas
authors.initials: N
authors.lastname: Verheyen
authors.forename: Femke
authors.initials: F
authors.lastname: Rutters
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Dekker
authors.forename: Stefan
authors.initials: S
authors.lastname: Pilz
mesh_terms: D001842:Bone and Bones / Q000378:metabolism / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D018167:Receptors, Calcitriol / Q000235:genetics; D012084:Renin-Angiotensin System; D012307:Risk Factors; D014807:Vitamin D / Q000235:genetics / Q000378:metabolism*; D014808:Vitamin D Deficiency / Q000150:complications / Q000235:genetics / Q000473:pathology
chemical_list: D018167:Receptors, Calcitriol; D014807:Vitamin D