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Excitatory effect of Clostridium perfringens alpha toxin on the rat isolated aorta
Author(s) -
Fujii Yoshio,
Nomura Shigemasa,
Oshita Yoshitami,
Sakurai Jun
Publication year - 1986
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.1476-5381.1986.tb10233.x
Subject(s) - clostridium perfringens , alpha (finance) , toxin , excitatory postsynaptic potential , aorta , chemistry , microbiology and biotechnology , biology , medicine , neuroscience , bacteria , inhibitory postsynaptic potential , surgery , construct validity , patient satisfaction , genetics
1 Clostridium perfringens alpha toxin caused contraction of the isolated aorta of the rat in a dose‐dependent manner. 2 The contractile action caused by the toxin was inhibited or abolished by calcium antagonists such as nifedipine, verapamil and cinnarizine, or a Ca‐free medium, but was not affected by phentolamine, chlorpheniramine, atropine, tetrodotoxin or a low Na medium. 3 The toxin stimulated Ca uptake into the aorta in a dose‐dependent manner. 4 8‐N,N'‐diethylaminooctyl‐3,4,5‐trimethoxybenzoate (TMB‐8) blocked significantly both the toxin‐ and noradrenaline (NA)‐induced contractions. 5 Trifluoperazine (TFP) and N‐(6‐aminohexyl)‐5‐chloro‐l‐naphtharene sulphonamide (W‐7) did not affect the contractile activity of the toxin but blocked the NA‐induced contraction. 6 The toxin also stimulated the 32 P phosphate labelling of phosphatidylinositol (PI) and phosphatidic acid (PA) in the preparation. 7 These results indicate that the toxin‐induced contraction, which is different from that induced by NA, is the result of a direct action of the toxin on the aorta and is due to an increased Ca 2+ permeability across the smooth muscle membrane. It is suggested that the contractile response to the toxin is associated with activation of phospholipid metabolism and enhanced entry of Ca into the aorta.