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Chlorpromazine and diltiazem effects in muscle: blockage of acetylcholine-evoked contractures, membrane currents and tracer calcium uptake.

Contractures evoked by 0.1 mmol/l acetylcholine (ACh) in bundles from mouse soleus muscles denervated for 3-7 days were partly inhibited for more than 1 h following 2- to 10-min exposure to 10-100 mumol/l chlorpromazine (CP). The effect was stronger in sucrose than in Na+ solutions. A prolonged ACh-contracture blockage by diltiazem (20 mumol/l) was found only in the sucrose solution. Membrane currents evoked by ACh in the absence of Na+ were blocked by both the drugs, but recovered to more than 60% within 1 min of drug washout. ACh-evoked retention of tracer 45Ca2+ was decreased by more than 90 or 70% when CP or diltiazem, respectively, were applied and washed away 10 min before addition of 45Ca2+ and ACh. The results suggest that the prolonged contracture blockage was not related to the blockage of ionic currents through the ACh-receptor channel but to a drug-induced loss of Ca(2+)-storing capacity.