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Author Blockade, Ii P.-Adrenoreceptor ♦ Prolongsactionpotentialduration, Ill ♦ Sodpjm R. A. I., A. ♦ Sheldon, Robert S. ♦ Hill, Roger J. ♦ Duft, Henry J.
Source CiteSeerX
Content type Text
File Format PDF
Subject Domain (in DDC) Computer science, information & general works ♦ Data processing & computer science
Subject Keyword Cardiac Sodium Channel ♦ Current Model ♦ Sodium Channel ♦ Rat Cardiac Myocyte Sodium Channel ♦ Impulse Propagation ♦ Action Potential ♦ Electrophysiological Study ♦ Recent Radioligand Study ♦ Predicted Receptor ♦ Batrachotoxinin-a Benzoate ♦ Binding Site ♦ Major Electrophysiological Effect ♦ Relevant Concentra-tions ♦ Initial Depolarization ♦ Widespread Use ♦ Antiarrhyth-mic Drug ♦ Similar Rank Order
Abstract The major electrophysiological effect of Class I antiarrhyth-mic drugs is blockade of the cardiac sodium channel, thereby reducing the initial depolarization of the action potential and slowing impulse propagation. Despite the widespread use of these drugs our understanding of their mechanism of action is incomplete. Models based on electrophysiological studies predict that a receptor for Class I drugs is associated with the sodium channel, and that occupancy of this receptor causes blockade of the sodium channel. Recent radioligand studies with [3H]batrachotoxinin-A benzoate have identified a binding site for Class I drugs associated with rat cardiac myocyte sodium channels, which may be the predicted receptor. Binding of drugs to this site is saturable, reversible, stereo-specific, and occurs at pharmacologically relevant concentra-tions with similar rank order of potency in vivo and in vitro.
Educational Role Student ♦ Teacher
Age Range above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study