Key result
Diphenylamine-2-carboxylate caused a dose-related increase in membrane resistance in rat skeletal muscle fibres due to a fall in C1- channel conductance (IC50, 120 microM).
DPC blocks C1- channel conductance and modifies excitability in rat skeletal muscle, though less potently than in C1- transporting epithelia.
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Does not alter clinical practice; extends epithelial Cl- blockade data to rat skeletal muscle with lower potency.
The effect of diphenylamine-2-carboxylate (DPC), a blocker of the C1- conductive pathway in C1- transporting epithelia, has been evaluated in-vitro on the electrophysiological variables of rat extensor digitorum longus muscle fibres. DPC (5-240 microM) caused a dose-related increase of membrane resistance which was attributed entirely to a fall in C1- channel conductance (IC50, 120 microM), since potassium conductance was not affected by the treatment. DPC also modified fibre excitability. A significant dose-dependent increase was observed in the latency of the action potential and in the excitability of the membrane. DPC was less potent on striated fibres than anthracene-9-carboxylic acid, another specific blocker of C1- channel conductance. Moreover DPC was less potent on skeletal muscle than on C1- transporting epithelia. Morphological differences in the C1- channels or of the drug binding sites may account for the differences between tissues.
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Camerino et al. (1989) studied this question. Diphenylamine-2-carboxylate (DPC) was evaluated on C1- channel conductance (IC50 120 microM). Diphenylamine-2-carboxylate caused a dose-related increase in membrane resistance in rat skeletal muscle fibres due to a fall in C1- channel conductance (IC50, 120 microM).
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