Abstract
The intravenous pretreatment with enkephalinase inhibitors KB 101 and acetorphan increased the heart resistance to the arrhythmogenic action of adrenaline (epinephrine), is related to activation of the delta-opioid receptors by endogenous enkephalins. At the same time, the mu-receptors and their endogenous agonists play an insignificant role in development of the antiarrhythmic effect of acetorphan. The enkephalinase inhibitors are a promising group of compounds for the development of new antiarrhythmic drugs, because these agents, in contrast to opiates, do not lead to narcotic addiction.
MeSH terms
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Animals
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Anti-Arrhythmia Agents / pharmacology*
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Arrhythmias, Cardiac / chemically induced
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Arrhythmias, Cardiac / prevention & control
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CD13 Antigens / antagonists & inhibitors
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Disulfides / pharmacology
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Enzyme Inhibitors / pharmacology*
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Epinephrine
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Male
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Neprilysin / antagonists & inhibitors*
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Phenylalanine / analogs & derivatives*
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Phenylalanine / pharmacology
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Rats
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Rats, Wistar
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Receptors, Opioid, delta / agonists
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Receptors, Opioid, mu / agonists
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Thiorphan / analogs & derivatives*
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Thiorphan / pharmacology
Substances
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Anti-Arrhythmia Agents
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Disulfides
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Enzyme Inhibitors
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Receptors, Opioid, delta
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Receptors, Opioid, mu
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RB 101
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Phenylalanine
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racecadotril
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Thiorphan
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CD13 Antigens
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Neprilysin
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Epinephrine