Oxidative Stress in Arterial Hypertension

• Guillermo Zalba

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

• Gorka San José

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

• María U. Moreno

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

• María A. Fortuño

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

• Ana Fortuño

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

• Francisco J. Beaumont

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

• Javier Díez

  From the Division of Cardiovascular Pathophysiology, School of Medicine (G.Z., G.S.J., M.U.M., M.A.F., A.F., F.J.B., J.D.), and the Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain.

書誌事項

タイトル別名

• Role of NAD(P)H Oxidase

抄録

Increased vascular reactive oxygen species production, especially superoxide anion, contributes significantly in the functional and structural alterations present in hypertension. An enhanced superoxide production causes a diminished NO bioavailability by an oxidative reaction that inactivates NO. Exaggerated superoxide levels and a low NO bioavailability lead to endothelial dysfunction and hypertrophy of vascular cells. It has been shown that the enzyme NAD(P)H oxidase plays a major role as the most important source of superoxide anion in vascular cells. Several experimental observations have shown an enhanced superoxide generation as a result of the activation of vascular NAD(P)H oxidase in hypertension. Although this enzyme responds to stimuli such as vasoactive factors, growth factors, and cytokines, some recent data suggest the existence of a genetic background modulating the expression of its different components. New polymorphisms have been identified in the promoter of the p22 phox gene, an essential subunit of NAD(P)H oxidase, influencing the activity of this enzyme. Genetic investigations of these polymorphisms will provide novel markers for determination of genetic susceptibility to oxidative stress in hypertension.

収録刊行物

• Hypertension

  Hypertension 38 (6), 1395-1399, 2001-12

  Ovid Technologies (Wolters Kluwer Health)

キーワード

• Internal Medicine

詳細情報

• CRID: 1363388843719232768
• NII論文ID: 30029739254
• DOI: 10.1161/hy1201.099611
• ISSN: 15244563
• ISSN: 0194911X
• ISSN: http://id.crossref.org/issn/0194911X
• Web Site: https://www.ahajournals.org/doi/full/10.1161/hy1201.099611
• データソース種別:
  • Crossref
  • CiNii Articles