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Shear stress‐induced vasodilation does not increase eNOS phosphorylation at ser1179
Author(s) -
Wolfert Madeline,
Harris M. Brennan,
LooftWilson Robin
Publication year - 2007
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.21.6.a858
Subject(s) - enos , shear stress , vasodilation , chemistry , medicine , anatomy , constriction , endocrinology , cardiology , biophysics , nitric oxide synthase , nitric oxide , materials science , biology , composite material
Increased shear stress has been shown to augment endothelial nitric oxide synthase (eNOS) activation in cultured endothelial cells, in part by phosphorylation at serine 1179 (S1179). However, there is little evidence that the same response occurs in intact vessels. Therefore, we hypothesized that an acute increase in shear stress in murine carotid arteries, sufficient to induce near maximal dilation, would result in augmented eNOS phosphorylation at S1179. Carotid arteries of C57BL/6 mice were isolated, cannulated, and pressurized to 80 mmHg. Arteries were pre‐constricted with phenylephrine (10 −5 M), then placed under conditions of either no shear stress (control) or high luminal shear stress (8‐18 dynes/cm 2 ), sufficient to produce near maximal dilation, for ~1, 10, or 30 min, then rapidly frozen. Additional arteries were treated with no shear stress or high shear stress (4‐20 dynes/cm 2 ) for 15 min without pre‐constriction. Western blotting revealed no difference in levels of phospho‐Ser1179‐eNOS between no shear stress and high shear stress treated arteries. Therefore, our results indicate that acute shear stress‐induced vasodilation in intact carotid arteries involves an alternate mechanism which may be different than those observed in cultured cells. Supported by NHLBI and HHMI‐UBSEP.