TY - JOUR
T1 - Bradykinin induces superoxide anion release from human endothelial cells
AU - Holland, James A.
AU - Pritchard, Kirkwood A.
AU - Pappolla, Miguel A.
AU - Wolin, Michael S.
AU - Rogers, Nancy J.
AU - Stemerman, Michael B.
PY - 1990/4
Y1 - 1990/4
N2 - The time‐dependent release of superoxide anion (O 2−) from bradykinin (Bk)‐stimulated human umbilical vein endothelial cells (EC) was measured as the superoxide dismutase‐inhibitable reduction of ferricytochrome C employing a novel application of microspectrophotometry. In the absence of Bk, O 2− release by EC was not detectable. EC exposure to Bk (10−6 to 10−5 M) resulted in a rapid release of O 2−. The release of O 2− occurred within 5 minutes of exposure. O 2− release was partially inhibited by indomethacin (63 ± 6%), thus suggesting that arachidonic acid metabolism, through cyclooxygenase, contributes to EC O 2− production. EC O 2− release may be an important component in the pathophysiologic actions of Bk on vascular function.
AB - The time‐dependent release of superoxide anion (O 2−) from bradykinin (Bk)‐stimulated human umbilical vein endothelial cells (EC) was measured as the superoxide dismutase‐inhibitable reduction of ferricytochrome C employing a novel application of microspectrophotometry. In the absence of Bk, O 2− release by EC was not detectable. EC exposure to Bk (10−6 to 10−5 M) resulted in a rapid release of O 2−. The release of O 2− occurred within 5 minutes of exposure. O 2− release was partially inhibited by indomethacin (63 ± 6%), thus suggesting that arachidonic acid metabolism, through cyclooxygenase, contributes to EC O 2− production. EC O 2− release may be an important component in the pathophysiologic actions of Bk on vascular function.
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U2 - 10.1002/jcp.1041430104
DO - 10.1002/jcp.1041430104
M3 - Article
C2 - 2156873
AN - SCOPUS:0025306418
SN - 0021-9541
VL - 143
SP - 21
EP - 25
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
IS - 1
ER -