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Calcitriol protects renovascular function in hypertension by down-regulating angiotensin II type 1 receptors and

Jinghui Dong1, Siu Ling Wong, Chi Wai Lau

  • 1Institute of Vascular Medicine, Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, China.

European Heart Journal
|January 24, 2012
PubMed
Abstract

Insights

Calcitriol, an active form of vitamin D, improves blood vessel function in hypertension by reducing harmful reactive oxygen species (ROS) and normalizing protein expression. This suggests calcitriol effectively preserves endothelial function in hypertensive conditions.

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Vascular Biology

Background:

  • Hypertension is associated with renovascular dysfunction and impaired endothelial function.
  • Oxidative stress, indicated by reactive oxygen species (ROS), plays a critical role in vascular dysfunction.
  • The active form of vitamin D, calcitriol, is being investigated for its potential protective effects on the vasculature.

Purpose of the Study:

  • To determine if calcitriol protects against renovascular dysfunction in hypertension.
  • To investigate whether calcitriol alters the expression of key proteins involved in hypertension-induced vascular dysfunction.

Main Methods:

  • In vitro and in vivo studies using renal arteries from hypertensive patients and spontaneously hypertensive rats (SHR).
  • Isometric tension measurements to assess vascular reactivity.
  • Dihydroethidium fluorescence to quantify ROS levels.
  • Immunofluorescence to analyze protein expression (AT(1)R, NOX, SOD).
  • Administration of calcitriol and a vitamin D receptor (VDR) antagonist (TEI-9647).

Main Results:

  • Calcitriol enhanced endothelium-dependent relaxations and reduced ROS in renal arteries of hypertensive patients.
  • Calcitriol treatment decreased the expression of AT(1)R, NOX-2, NOX-4, and p67(phox), while increasing SOD-1.
  • In vivo and in vitro calcitriol administration normalized vascular function, ROS levels, and protein expression in hypertensive rat models.
  • The effects of calcitriol were abolished by a VDR antagonist, confirming VDR mediation.

Conclusions:

  • Calcitriol, through VDR activation, improves endothelial function in hypertension.
  • Calcitriol normalizes the expression of angiotensin II type 1 receptor (AT(1)R) and enzymes involved in radical generation and scavenging.
  • Calcitriol effectively prevents ROS over-production and preserves endothelial function in hypertensive states.

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