[Sodium channel blocking effect of scorpion venom on cultured mouse myocardiocytes].
Myocardiocytes of mice were cultured. Action potentials were recorded with microelectrodes inside the cells. Scorpion venom from Buthus martensii Karsch 3.75 or 7.5 micrograms.ml-1 decreased the duration of action potential and all of the depolarization concerned parameters of myocardiocytes. The Vmax, TP, APA behaved apparently in a dosage-dependent way. Restoration happened after washing out. Tetrodotoxin 2.5 micrograms.ml-1 acted in a similar way. Nimodipine 3.0 micrograms.ml-1 led to a decrease in action potential duration. BaCl2 0.1 mmol.L-1 elongated the action potential duration, while decreased the parameters concerned with depolarization. These results indicate that the scorpion venom has Na+ channel blocking action.
Qi
H
H
Department of Physiology, Norman Bethune University of Medical Sciences, Changchun, China.
Zhong
G G
GG
Chen
L
L
Jiang
Y
Y
Wei
J J
JJ
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D002478:Cells, Cultured; D002712:Chlorides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000187:drug effects*; D051379:Mice; D009206:Myocardium / Q000166:cytology; D009553:Nimodipine / Q000494:pharmacology; D012604:Scorpion Venoms / Q000494:pharmacology*; D015222:Sodium Channels / Q000187:drug effects*; D013779:Tetrodotoxin / Q000494:pharmacology
D017609:Barium Compounds; D002712:Chlorides; D012604:Scorpion Venoms; D015222:Sodium Channels; C024986:barium chloride; D013779:Tetrodotoxin; D009553:Nimodipine