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Nox‐4 siRNA Causes Attenuation of Hypoxic Pulmonary Vasoconstriction in Bovine Pulmonary Arteries
Author(s) -
Ahmad Mansoor,
Kelly Melissa R,
Kandhi Sharath,
Zhao Xiangmin,
Wolin Michael S
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1002.8
Subject(s) - superoxide , hypoxic pulmonary vasoconstriction , chemistry , nox , apocynin , vasoconstriction , endothelium , hydrogen peroxide , pharmacology , medicine , biochemistry , organic chemistry , combustion , enzyme
Hypoxic pulmonary vasoconstriction (HPV) in endothelium removed bovine pulmonary arteries (BPA) is potentially mediated through the removal of a superoxide‐derived hydrogen peroxide mediated basal relaxation. To study the source of the superoxide, endothelium removed BPA rings were cultured for 48 hrs with the first 24 in the presence of either Nox‐4 or Nox‐2 siRNA. Nox‐4 siRNA caused a significant decrease in Nox‐4 expression without any effect on Nox‐2 levels. Superoxide levels and HPV were significantly reduced in BPA rings treated with Nox‐4 siRNA without affecting force development to KCl. Superoxide levels were significantly reduced with Nox‐2 siRNA treatment however, HPV and KCl force were not affected. Endothelium removed BPA rings treated with apocynin and gp91‐dstat show a decrease in superoxide levels but did not affect either KCl force or HPV. Thus Nox‐4 and not Nox‐2 may be the source for the potential superoxide derived peroxide mechanism maintaining basal relaxation during normoxia which when removed leads to HPV. Support by NIH grants HL31069, HL43023 and HL66331.