The action of benzalkonium chloride on the activation of contraction in frog skeletal muscle.
Toe muscle was used. The changes in K contracture and in the resting potential were measured. Above 0.2 mM, benzalkonium-Cl (BAC) induced an irreversible  contracture associated to a rapid depolarization which caused in few min. the abolition  of K contractures. With 0.5 mM, a steady tension representing 13-40% of maximal K contractures was reached in 11-16 sec. The development of BAC rigor was delayed in K depolarized muscles. BAC rigor had similarly a slower development after destruction of transverse tubules, suggesting a direct effect on sarcoplasmic reticulum (SR) in the maintenance of the steady tension and the dependence on membrane depolarization of its rapid onset. BAC effects were not affected by 10(-4) M D-tubocurarine. Concentrations between 0.01 and 0.2 mM induced within tens of min. the irreversible depolarization and abolition of K contractures. Caffeine contracture was diminished. Pretreatment with lower concentrations favoured the development of BAC rigor in K depolarized muscles. These findings suggest that even in lower concentrations, besides the depolarizing and the uncoupling effects, BAC is still able to depress Ca uptake by SR.
D000818:Animals; D001001:Anura; D001548:Benzalkonium Compounds / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects*; D011893:Rana esculenta
D001548:Benzalkonium Compounds