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Role of Superoxide in endothelium‐dependent dilation of soleus feed arteries in young and old rats
Author(s) -
Trott Daniel Wayne,
Seawright John W,
Woodman Christopher R
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.602.2
Subject(s) - tiron , vasodilation , acetylcholine , chemistry , superoxide , dilator , medicine , nitric oxide , endocrinology , vasoconstriction , endothelium , biochemistry , enzyme
We tested the hypothesis that superoxide (O 2 − ) contributes to age‐induced endothelial dysfunction in rat soleus feed arteries (SFA). SFA from young (4 mo) and old (24 mo) Fischer 344 rats were isolated and cannulated for examination of vasodilator responses to flow and acetylcholine (ACh) in the absence or presence of an NAD(P)H oxidase inhibitor (DPI; 10μM) or a O 2 − scavenger (Tiron; 10mM). Flow‐ and ACh‐induced dilations were attenuated in old SFA. Addition of DPI and Tiron improved flow‐ but not Ach‐induced dilation in old SFA. In young SFA, DPI and Tiron had no effect on flow‐induced dilation and attenuated ACh‐induced dilation. To determine if O 2 − contributes to endothelium derived hyperpolarizing factor‐ (EDHF) mediated, ACh‐induced dilation, dilator responses were assessed in the presence of L‐NNA (300μM), indomethacin (5μM), and/or Tiron. In young SFA, incubation with L‐NNA+Indo+Tiron attenuated ACh‐induced dilation to a greater extent than L‐NNA+Indo or Tiron alone. Immunobloting revealed that protein content of NAD(P)H subunits gp91phox and p67phox were greater in old SFA compared to young. These results suggest that O 2 − contributes to impaired flow‐induced dilation in old SFA. In contrast O 2 − appears to play a role EDHF mediated dilation in response to ACh. Supported by AHA 0765043Y, and a Huffines Institute Research Grant.