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Contraction of the rat isolated aorta caused by Clostridium perfringens alpha toxin (phospholipase C): evidence for the involvement of arachidonic acid metabolism
Author(s) -
Fujii Yoshio,
Sakurai Jun
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.tb11931.x
Subject(s) - arachidonic acid , clostridium perfringens , contraction (grammar) , thromboxane a2 , toxin , biology , pharmacology , endocrinology , chemistry , biochemistry , medicine , receptor , enzyme , genetics , bacteria
1 Alpha toxin produced by Clostridium perfringens contracted the rat isolated aorta and stimulated release of arachidonic acid in the tissue. 2 Quinacrine did not inhibit contraction caused by the toxin. 3 Indomethacin blocked contraction caused by the toxin in a dose‐dependent manner and markedly increased levels of arachidonic acid released by the toxin. 4 The toxin‐induced contraction was blocked by the thromboxane synthetase inhibitor OKY‐046 and the thromboxane A 2 (TXA 2 ) antagonist ONO‐3708. 5 The toxin stimulated production of TXB 2 and this was blocked by pretreatment with either indomethacin or OKY‐046. 6 Toxin‐induced contraction was diminished by pretreating aorta with collagenase or by rubbing the intimal surface to remove the endothelium. 7 These data suggest that the contractile response to the toxin is associated with stimulation of TXA 2 production from arachidonic acid released by the toxin in the endothelial cells of the aorta.