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Angiogenesis in the Ischemic Rat Lung
07:36

Angiogenesis in the Ischemic Rat Lung

Published on: February 8, 2013

[Inflammatory injurious effect of angiotensin II on pulmonary microvascular endothelium in rat]

Hong Zhang1, Geng-Yun Sun

  • 1Department of Emergency, First Affiliated Hospital, Anhui Medical University, Hefei 230061, Anhui, China.

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue = Chinese Critical Care Medicine = Zhongguo Weizhongbing Jijiuyixue
|October 6, 2004
PubMed
Abstract

Insights

Angiotensin II (AngII) worsens lung microvascular endothelial cell injury caused by lipopolysaccharide (LPS). Blocking the Angiotensin II type 1 receptor prevents this combined damage, suggesting a therapeutic target.

Area of Science:

  • Pulmonary vascular research
  • Endothelial cell biology
  • Cardiovascular pharmacology

Context:

  • Pulmonary microvascular endothelial cells (RPMVECs) form a critical barrier in the lungs.
  • Endothelial barrier dysfunction is implicated in acute lung injury.
  • Angiotensin II (AngII) plays a role in vascular regulation and inflammation.

Purpose:

  • To investigate the synergistic effects of AngII and lipopolysaccharide (LPS) on RPMVEC monolayer permeability.
  • To determine if blocking the Angiotensin II type 1 receptor can prevent AngII and LPS-induced endothelial injury.

Summary:

  • Lipopolysaccharide (LPS) significantly increased RPMVEC monolayer permeability.
  • Angiotensin II (AngII) exacerbated LPS-induced permeability, indicating a synergistic injurious effect.
  • (Sar1, Ile8)-Ang II, an Angiotensin II type 1 receptor antagonist, significantly prevented this synergistic damage.

Impact:

  • This study highlights the detrimental interaction between AngII and LPS in the pulmonary endothelium.
  • Targeting the Angiotensin II type 1 receptor may offer a therapeutic strategy to mitigate LPS-induced lung injury.
  • Findings contribute to understanding endothelial dysfunction in critical care settings.

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