Abstract
Actions of myosin light chain kinase inhibitors were tested on delayed rectifier potassium current (IK) in dissociated bullfrog sympathetic neurons. A microbial product, wortmannin (10 microM, extracellularly) and a synthetic peptide, SM-1 (20 microM, intracellularly) caused approximately 35 mV hyperpolarizing shift of the inactivation curve. Substitution of ATP (1.15 mM) in the pipette solution with 5'-adenylylimidodiphosphate mimicked the actions of wortmannin and SM-1. Results suggest that phosphorylation of myosin may modulate kinetics for the inactivation of IK.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenylyl Imidodiphosphate / pharmacology
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Androstadienes / pharmacology
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Animals
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Electrophysiology
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Enzyme Inhibitors / pharmacology
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Ganglia, Sympathetic / cytology
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Ganglia, Sympathetic / drug effects
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In Vitro Techniques
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Myosin-Light-Chain Kinase / antagonists & inhibitors*
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Myosin-Light-Chain Kinase / pharmacology
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Neurons / drug effects
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Neurons / metabolism*
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Peptide Fragments / pharmacology
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Potassium Channels / drug effects
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Potassium Channels / metabolism*
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Rana catesbeiana
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Sympathetic Nervous System / cytology
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Sympathetic Nervous System / drug effects
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Sympathetic Nervous System / metabolism*
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Wortmannin
Substances
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Androstadienes
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Enzyme Inhibitors
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Peptide Fragments
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Potassium Channels
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SM 1 peptide
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Adenylyl Imidodiphosphate
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Myosin-Light-Chain Kinase
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Wortmannin