Trifluoperazine and the rapid, Ca2+-triggered damage of skeletal and cardiac muscle.
[Ca2+]i was raised experimentally in mammalian and amphibian skeletal and cardiac muscles by A23187, DNP, anoxia or the Ca2+ -paradox. Trifluoperazine (TFP) at 10(-5) M failed to protect against the characteristic and rapid damage triggered by elevated [Ca2+]i in any of the preparations. It is concluded that calmodulin is not implicated in this rapid ultrastructural damage. TFP alone also causes identical patterns of damage. It may be acting to raise [Ca2+]i in skeletal and cardiac muscle cells.
D000818:Animals; D000001:Calcimycin / Q000633:toxicity; D002118:Calcium / Q000633:toxicity*; D003327:Coronary Disease / Q000517:prevention & control*; D004140:Dinitrophenols / Q000633:toxicity; D000860:Hypoxia / Q000503:physiopathology; D051379:Mice; D009135:Muscular Diseases / Q000517:prevention & control*; D011896:Rana temporaria; D013347:Subcellular Fractions / Q000187:drug effects; D014268:Trifluoperazine / Q000627:therapeutic use*
D004140:Dinitrophenols; D014268:Trifluoperazine; D000001:Calcimycin; D002118:Calcium