Abstract
The effect of the antiarrhythmic drug amiodarone on the human myocardial beta-adrenoceptor-G protein-adenylyl cyclase signalling cascade was investigated. Amiodarone had no effect on myocardial G proteins and maximal adenylyl cyclase activity, but acted as a beta-adrenoceptor antagonist. This mechanism might be at least partially responsible for the beneficial effects of the drug in patients with arrhythmia and heart failure.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenylyl Cyclases / metabolism
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Adrenergic beta-Agonists / pharmacology
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Adrenergic beta-Antagonists
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Amiodarone / therapeutic use*
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Animals
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Anti-Arrhythmia Agents / therapeutic use*
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GTP-Binding Proteins / drug effects*
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GTP-Binding Proteins / metabolism
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Heart / drug effects*
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Heart Failure / drug therapy*
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Humans
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Isoproterenol / pharmacology
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Myocardium / enzymology
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Myocardium / metabolism*
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Radioligand Assay
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Rats
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Rats, Sprague-Dawley
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Receptors, Adrenergic, beta / drug effects*
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Receptors, Adrenergic, beta / metabolism
Substances
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Adrenergic beta-Agonists
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Adrenergic beta-Antagonists
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Anti-Arrhythmia Agents
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Receptors, Adrenergic, beta
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GTP-Binding Proteins
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Adenylyl Cyclases
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Isoproterenol
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Amiodarone