Vitamin D-RAAS Connection: An Integrative Standpoint into Cardiovascular and Neuroinflammatory Disorders

Curr Protein Pept Sci. 2020;21(10):948-954. doi: 10.2174/1389203721666200606220719.

Abstract

Background: The neuroinflammatory process is associated with the pathogenesis of many cardiovascular disorders, particularly with hypertension. In this regard, the deficiency of vitamin D seems to increase the risk of cardiovascular pathologies related to neuroinflammation. Long-term lack of vitamin D leads to over-activation of the renin-angiotensin-aldosterone system (RAAS), one of the essential mechanisms of blood pressure regulation.

Purpose of review: This review summarizes the latest studies carried out to evaluate the primary mechanisms underlying the neuroprotective effect of vitamin D and its receptors (VDR) in the central nervous system. Besides, the present article condenses the evidence supporting the link between vitamin D and the RAAS in hypertension and neuroinflammation. Highlights Standpoints: Vitamin D deficiency is highly prevalent in the world, and the rising prevalence of neuroinflammatory diseases and associated pathologies such as hypertension around the world justifies the urgent need of searching new and more effective therapeutic methods that could be related to RAAS modulation and vitamin D levels management.

Keywords: VDR; Vitamin D; hypertension; neuroinflammation; oxidative stress; renin-angiotensin-aldosterone system.

Publication types

  • Review

MeSH terms

  • Angiotensin II Type 1 Receptor Blockers / therapeutic use
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Central Nervous System / drug effects
  • Central Nervous System / metabolism
  • Central Nervous System / pathology
  • Gene Expression Regulation
  • Humans
  • Hypertension / drug therapy
  • Hypertension / genetics
  • Hypertension / metabolism*
  • Hypertension / pathology
  • Inflammation
  • Oxidative Stress / drug effects
  • Peptidyl-Dipeptidase A / genetics
  • Peptidyl-Dipeptidase A / metabolism*
  • Receptor, Angiotensin, Type 1 / genetics
  • Receptor, Angiotensin, Type 1 / metabolism*
  • Receptors, Calcitriol / genetics
  • Receptors, Calcitriol / metabolism*
  • Receptors, Tumor Necrosis Factor, Type I / genetics
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Renin-Angiotensin System / drug effects
  • Renin-Angiotensin System / genetics
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Vitamin D / metabolism*
  • Vitamin D / therapeutic use
  • Vitamin D Deficiency / drug therapy
  • Vitamin D Deficiency / genetics
  • Vitamin D Deficiency / metabolism*
  • Vitamin D Deficiency / pathology

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Angiotensin-Converting Enzyme Inhibitors
  • Receptor, Angiotensin, Type 1
  • Receptors, Calcitriol
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha
  • VDR protein, human
  • Vitamin D
  • ACE protein, human
  • Peptidyl-Dipeptidase A