Regulation of the number of alpha-bungarotoxin binding sites in cultured chick myotubes by a 1,4 dihydropyridine calcium channel antagonist.
Calcium has been suggested as the second messenger link between skeletal muscle activity and AChR gene expression and synthesis. We have compared the concentrations of the Ca2+ channel antagonists D600 and nisoldipine needed both to block Ca2+ uptake into cultured myotubes and to increase AChR expression. The good correspondence between these two measurements and the use of the highly specific Ca2+ channel antagonist nisoldipine strengthens the hypothesis that AChR expression is regulated by levels of intracellular Ca2+.
Smilowitz
H
H
Department of Pharmacology, University of Connecticut Health Center, Farmington 06032.
Smart
E
E
Bowik
C
C
Chang
R J
RJ
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D002038:Bungarotoxins / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002478:Cells, Cultured; D002642:Chick Embryo; D005711:Gallopamil / Q000494:pharmacology*; D007700:Kinetics; D009132:Muscles / Q000378:metabolism*; D009543:Nifedipine / Q000031:analogs & derivatives / Q000494:pharmacology; D015737:Nisoldipine; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism*
D002038:Bungarotoxins; D002121:Calcium Channel Blockers; D011950:Receptors, Cholinergic; D005711:Gallopamil; D015737:Nisoldipine; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D002118:Calcium