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Paradoxical vasoconstrictive effects of H2S on shear stress‐mediated vasodilation
Author(s) -
Lee HonChi,
Chai Qiang,
Lu Tong,
Wang XiaoLi
Publication year - 2013
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.27.1_supplement.1185.2
Subject(s) - vasodilation , iberiotoxin , enos , medicine , chemistry , coronary arteries , endocrinology , shear stress , contraction (grammar) , vascular smooth muscle , artery , anatomy , biophysics , cardiology , nitric oxide , biology , smooth muscle , nitric oxide synthase , materials science , composite material
We examined the role of H 2 S on shear stress‐mediated dilation of isolated mouse coronary arteries. Na 2 S produced concentration‐dependent dilation in these vessels, which was significantly inhibited by iberiotoxin. BK currents in mouse coronary smooth muscle cells were directly activated by Na 2 S, suggesting H 2 S produced vasodilation through BK channel activation. Using a pressure servo controller system, freshly isolated mouse coronary arteries were subjected to physiological levels of shear stress (1 to 25 dynes/cm 2 ), producing graded dilatory responses, but such effects were diminished in the presence of 100 μM Na 2 S. Pre‐incubation with the cystathionine γ‐lyase inhibitor, D,L‐propargylglycine (PPG), resulted in a paradoxical augmentation of shear stress‐mediated vasodilation. However, in the presence of L‐NAME or in coronary arteries from eNOS knockout mice, PPG inhibited shear stress‐mediated vasodilation, suggesting an interaction between NO and H 2 S signaling. Using cultured bovine aortic endothelial cells, eNOS activity was inhibited by Na 2 S. These results suggest that both NO and H 2 S are important shear stress‐mediated vasodilators in mouse coronary arteries but there is a complex interaction between these two signaling pathways that results in paradoxical vasoconstrictive effects of H 2 S through inhibition of NO generation. (Supported by grants from NIH)