A study is being made of the pharmacology of ion exchange in skeletal muscles. Resting exchange of K42 is blocked rather selectively by inorganic cations (e.g Rb ion and Ba ions and by organic cations (e.g., 9-aminoacridine, AA9 ; tetraethylammonium; SKF 525-A; local anesthetics). The long range objective of this study is to further characterize the mechanisms whereby these drugs impair the uptake and loss of K42 by skeletal muscle. In addition, a study is being made of the pharmacology of transmitter release at the nerve-muscle junction. Among the drugs studied are those that affect release by modifying the nerve terminal action potential and those that do so by activating nerve terminal cholinoceptive sites. Both sites should bear upon the pharmacology of drugs used in the management of skeletal muscle disorders.