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Kinins act on B 1 or B 2 receptors to release conjointly endothelium‐derived relaxing factor and prostacyclin from bovine aortic endothelial cells
Author(s) -
D'OrléansJuste Pedro,
Nucci Gilberto,
Vane John R.
Publication year - 1989
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 - 10.1111/j.1476-5381.1989.tb11903.x
Subject(s) - bradykinin , prostacyclin , kinin , receptor , endocrinology , chemistry , medicine , receptor antagonist , antagonist , agonist , bradykinin receptor , endothelium , biology , biochemistry
1 Bradykinin (Bk) induced the coupled release of endothelium‐derived relaxing factor (EDRF) and prostacyclin (PGI 2 ) from bovine aortic endothelial cells grown in culture. The B 2 kinin receptor antagonist, [ d ‐Arg O ,Hyp 3 ,Thi 5,8 , d ‐Phe 7 ]‐Bk, abolished this release by Bk. 2 Des‐Arg 9 ‐Bk, a B 1 kinin receptor agonist, also induced the release of EDRF and PGI 2 , but much higher concentrations were required to obtain a similar release to that induced by Bk. 3 [Leu 8 ],des‐Arg 9 ‐Bk, a B 1 receptor antagonist, significantly reduced the response to des‐Arg 9 ‐Bk without affecting the release induced by Bk. 4 The release of EDRF and PGI 2 induced by arachidonic acid or ADP was not significantly affected by the B 2 or the B 1 antagonist. 5 We conclude, therefore, that Bk and des‐Arg 9 ‐Bk were acting respectively on B 2 and B 1 bradykinin receptors. 6 The possible role of kinin receptors in the release of EDRF and PGI 2 from endothelial cells is discussed.