Premium
Effect of juvenile growth on arteriolar eNOS phosphorylation
Author(s) -
Kang Lori S.,
Nurkiewicz Timothy R.,
Wu Guoyao,
Boegehold Matthew A.
Publication year - 2010
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.24.1_supplement.976.9
Subject(s) - enos , phosphorylation , medicine , nitric oxide , endocrinology , protein kinase b , endothelium , arteriole , juvenile , chemistry , biology , microbiology and biotechnology , nitric oxide synthase , circulatory system , genetics
Nitric oxide (NO) often contributes little to endothelium‐dependent dilation of arterioles in the young but mediates a large portion of these responses in adults. The aim of this study was to identify the mechanism by which NO emerges as an important endothelial factor in arterioles during juvenile growth. NO release in response to endothelium‐dependent agonists (ACh, A23187) was 5 to 6‐fold higher in gracilis muscle arterioles from 42–46 day‐old rats than in those from 25–28 day‐old rats. However, there were no differences between age groups in arteriolar wall eNOS expression or levels of the eNOS co‐factor BH 4 , and L‐Arg levels were actually lower in the older vessels than in the younger vessels (104 ± 6 vs.126 ± 3pmol/mg, p<0.05). In contrast, agonist‐induced phosphorylation of eNOS at its Ser 1177 residue was almost 75% higher in arterioles from 42–46 day‐old rats than in those from 25–28 day‐old rats. Arterioles from the older rats did not show increased expression of Akt/PKB or PKA, kinases that mediate eNOS Ser phosphorylation, or heat shock protein 90 (Hsp90), which facilitates this process. These findings indicate that eNOS becomes more susceptible to activation during growth due to a change in the regulation of its phosphorylation status, possibly reflecting increased kinase or Hsp90 activity rather than expression. Support: AHA 0755264B, 09GRNT2250298 (MAB); AHA 0755024Y (GW); NIH ES015022, ES018274 (TRN).