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.
Lorković
H
H
Abteilung für Allgemeine Physiologie, Universität Ulm, Deutschland.
Jäger
U
U
D000109:Acetylcholine / Q000633:toxicity; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002746:Chlorpromazine / Q000494:pharmacology*; D004110:Diltiazem / Q000494:pharmacology*; D018492:Dopamine Antagonists / Q000494:pharmacology*; D004594:Electrophysiology; D005260:Female; D007553:Isotope Labeling; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008807:Mice, Inbred BALB C; D009119:Muscle Contraction / Q000187:drug effects; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D013395:Sucrose / Q000378:metabolism
D002121:Calcium Channel Blockers; D018492:Dopamine Antagonists; D013395:Sucrose; D012964:Sodium; D004110:Diltiazem; D000109:Acetylcholine; D002118:Calcium; D002746:Chlorpromazine