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Peroxide mediates abnormal nitric oxide production in aged rat arteries
Author(s) -
Zhou Xiaosun,
Bohlen H Glenn,
Unthank Joseph L,
Miller Steven J
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.595.1
Subject(s) - nitric oxide , medicine , endocrinology , basal (medicine) , apocynin , chemistry , mesenteric arteries , catalase , oxidative stress , artery , nadph oxidase , insulin
Vascular oxidant stress increases with age and may cause dysregulation of the nitric oxide (NO) system. Our previous results have shown increased basal but suppressed flow‐mediated production of NO in aged resistance arteries that is corrected by antioxidant treatment. This study tested the hypothesis that H2O2 mediates abnormal NO production in resistance arteries of retired breeder (RB) rats. Animal groups consisted of young (Y) and RB Wistar Kyoto rats and RB pre‐treated with apocynin (RB+Apo). Microelectrodes were used to measure in vivo mesenteric artery H2O2 and NO simultaneously at baseline and during flow elevation by temporary occlusion of adjacent arteries. RB had significantly increased basal H2O2 compared with Y (15.6 ± 1.9 vs. 9.4 ± 0.9 uM, p< 0.05). Periarterial H2O2 levels were altered in proportion to flow changes in RB but not Y rats. In RB+Apo, H2O2 baseline was reduced to Y levels (8.2 ± 0.9 uM) and flow‐mediated H2O2 production inhibited. In RB, PEG‐catalase lowered baseline NO (1392 ± 211 to 576 ± 96 nM, p< 0.05) and restored flow‐mediated NO production (1060 ± 253 and 1826 ± 672 nM, 100 and 200% flow increase, respectively). The results suggest that elevated baseline and suppressed flow‐mediated NO production results from near maximal NO activation by H2O2 during aging, and imply that age‐related vascular dysfunction is not the result of reduced NO bioavailability. Support: HL42898 and HL20605.