NAD(P)H oxidase mediates angiotensin II-induced vascular macrophage infiltration and medial hypertrophy

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Jianhua Liu1, Fang Yang, Xiao-Ping Yang

  • 1Hypertension and Vascular Research Division and the Biostatistics Department, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, Mich 48202-2689, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|March 15, 2003
PubMed
Abstract

Insights

Angiotensin II (Ang II) increases vascular inflammation and growth by activating NAD(P)H oxidase. Inhibiting this enzyme reduces intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration without affecting blood pressure.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Vascular Biology

Background:

  • Reactive oxygen species (ROS) are implicated in Angiotensin II (Ang II)-induced intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration.
  • NAD(P)H oxidase is a key source of ROS and has been linked to cell growth and vascular hypertrophy.

Purpose of the Study:

  • To investigate the role of NAD(P)H oxidase in Ang II-induced ICAM-1 expression, macrophage infiltration, and vascular growth.
  • To determine if NAD(P)H oxidase inhibition attenuates these processes independently of blood pressure changes.

Main Methods:

  • Rats were infused with Ang II or vehicle, with or without a cell-permeant NAD(P)H oxidase inhibitor (gp91ds-tat peptide).
  • Immunohistochemical staining was used to assess ICAM-1 and ED1 (macrophage marker) expression.
  • Medial hypertrophy and blood pressure were measured.

Main Results:

  • Ang II significantly increased ICAM-1 expression, macrophage infiltration, and medial hypertrophy compared to vehicle.
  • Coinfusion with gp91ds-tat peptide attenuated these Ang II-induced effects.
  • The NAD(P)H oxidase inhibitor did not affect blood pressure.

Conclusions:

  • NAD(P)H oxidase activation by Ang II contributes to ICAM-1 expression, leukocyte infiltration, and vascular hypertrophy.
  • Inhibition of NAD(P)H oxidase offers a potential therapeutic strategy for vascular remodeling independent of blood pressure modulation.

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