Neuromuscular block after intra-arterially injected acetylcholine. 2. Effects of ACTH treatments as possible detectors of desensitization level in the receptor site.
It has been suggested that the effect of ACTH in myasthenia gravis may be ascribed to an action involving neuromuscular transmission which favours repolarization processes, with a tendency towards hyperpolarization of the membranes of muscle fibres and motor nerve endings. A similar mechanism has been postulated for the action of ACTH in epilepsy (Klein, 1970). A direct or indirect action on nerve membrane would interfere with depolarization. There is evidence of raised concentration of intracellular potassium and increased outflow of sodium ions which would cause hyperpolarization of the membrane. This paper studies the effect of ACTH on the late block of neuromuscular transmission caused by acetylcholine (ACTH).
D000109:Acetylcholine / Q000494:pharmacology*; D000200:Action Potentials; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology* / Q000627:therapeutic use; D004357:Drug Synergism; D004558:Electric Stimulation; D006801:Humans; D008475:Median Nerve / Q000187:drug effects / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects*; D009046:Motor Neurons / Q000187:drug effects; D009132:Muscles / Q000187:drug effects; D009157:Myasthenia Gravis / Q000188:drug therapy; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology*; D009469:Neuromuscular Junction / Q000187:drug effects*; D012032:Refractory Period, Electrophysiological; D009435:Synaptic Transmission / Q000187:drug effects*
D009467:Neuromuscular Depolarizing Agents; D000324:Adrenocorticotropic Hormone; D000109:Acetylcholine