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The involvement of reactive oxygen species and arachidonic acid in α 1 ‐adrenoceptor‐induced smooth muscle cell proliferation and migration
Author(s) -
Nishio Eisuke,
Watanabe Yasuhiro
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701171
Subject(s) - phenylephrine , vascular smooth muscle , catalase , reactive oxygen species , arachidonic acid , cell growth , microbiology and biotechnology , chemistry , chemotaxis , biology , endocrinology , biochemistry , medicine , oxidative stress , receptor , enzyme , smooth muscle , blood pressure
In a previous study, we demonstrated phenylephrine‐stimulated arachidonic acid (AA) release in rabbit cultured aortic smooth muscle cells. Therefore, we have investigated the functional implications of AA which are involved in the cellular response to phenylephrine, particularly proliferation and migration of rabbit cultured aortic smooth muscle cells. First, to determine whether AA directly modifies proliferation and mobility of vascular smooth muscle cells (VSMCs), we exposed the cells to AA. AA induced proliferation and migration of the cells in a dose‐dependent fashion. Concomitantly added catalase inhibited the proliferation and chemotaxis induced by AA of VSMCs. Conversely, aminotriazole enhanced the proliferation and migration induced by AA. Secondly, we investigated whether the proliferation and migration of VSMCs by phenylephrine were related to AA and hydrogen peroxide (H 2 O 2 ). The proliferation and chemotaxis of VSMCs by phenylephrine were inhibited by a phospholipase A 2 (PLA 2 ) inhibitor, or catalase. Lastly, we investigated the effects of AA and phenylephrine on the content of H 2 O 2 in VSMCs. AA and phenylephrine treatment led to an increase of H 2 O 2 in a dose‐dependent manner. These results suggest that the addition of phenylephrine to the cells caused the enhancement of proliferation and migration, probably by mediating AA release and reactive oxygen species (ROS) production.British Journal of Pharmacology (1997) 121 , 665–670; doi: 10.1038/sj.bjp.0701171