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

      Arteriosclerosis, Thrombosis, and Vascular Biology
      Aldehydes, analysis, Angiotensin II, pharmacology, Animals, Aorta, Thoracic, drug effects, pathology, Blood Pressure, Chemotaxis, Leukocyte, physiology, Enzyme Inhibitors, Gene Expression Regulation, Glycoproteins, Hypertrophy, Intercellular Adhesion Molecule-1, biosynthesis, genetics, Macrophages, cytology, enzymology, Male, Membrane Glycoproteins, antagonists & inhibitors, NADPH Oxidase, Rats, Rats, Sprague-Dawley, Reactive Oxygen Species, metabolism, Single-Blind Method, Tunica Intima, Tunica Media, Vasculitis, prevention & control

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          Abstract

          Our preliminary data suggested that angiotensin II (Ang II)-induced reactive oxygen species are involved in intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration in the rat thoracic aorta. Other reports demonstrating reactive oxygen species-induced cell growth suggested a potential role of NAD(P)H oxidase in vascular hypertrophy. In the present study, we postulate that NAD(P)H oxidase is functionally involved in Ang II-induced ICAM-1 expression, macrophage infiltration, and vascular growth, and that oxidase inhibition attenuates these processes independently of a reduction in blood pressure. Rats were infused subcutaneously with vehicle or Ang II (750 microg/kg per day) for 1 week in the presence or absence of gp91 docking sequence (gp91ds)-tat peptide (1 mg/kg per day), a cell-permeant inhibitor of NAD(P)H oxidase. Immunohistochemical staining for ICAM-1 and ED1, a marker of monocytes and macrophages, showed that both were markedly increased with Ang II compared with vehicle and were reduced in rats receiving Ang II plus gp91ds-tat. This effect was accompanied by an Ang II-induced increase in medial hypertrophy that was attenuated by coinfusion of gp91ds-tat; however, gp91ds-tat had no effect on blood pressure. Ang II-enhanced NAD(P)H oxidase plays a role in the induction of ICAM-1 expression, leukocyte infiltration, and vascular hypertrophy, acting independently of changes in blood pressure.

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