Effect of antiarrhythmic drugs, TTX, and 4-aminopyridine on repetitive electrical activity in frog skeletal muscle

P. Nánási, Miklós Dankó, David A. Lathrop

Research output: Contribution to journalArticle

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Abstract

1. Conventional microelectrode techniques were used to study the effects of antiarrhythmic drugs (quinidine, 2-20 μM; lidocaine, 5-50 μM; verapamil, 2-20 μM), 4-aminopyridine (4-AP, 50-100 μM), and tetrodotoxin (TTX, 1.5-6 nM) on repetitive electrical discharges induced in the muscle membrane in the presence of 1 μM cevadine. 2. Antiarrhythmic drugs and 4-AP produced progressive reduction of the maximum upstroke velocity (V+ max) of the discharges, while the cycle length was prolonged by each drug except 4-AP. 3. The efficacy in depression of V+ max and prolongation of cycle length was not proportional in the case of individual drugs. 4. A simple model of the repetitive activity incorporating drug-effects was presented. The cevadine-modified Na+ channels could be blocked by antiarrhythmic agents, however, the efficacy of these drugs on the normal and cevadine-modified Na+ channels were found to be different.

Original languageEnglish
Pages (from-to)563-567
Number of pages5
JournalGeneral Pharmacology
Volume21
Issue number4
DOIs
Publication statusPublished - 1990

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4-Aminopyridine
Veratrine
Anti-Arrhythmia Agents
Anura
Skeletal Muscle
Pharmaceutical Preparations
Quinidine
Tetrodotoxin
Microelectrodes
Verapamil
Lidocaine
Muscles
Membranes

ASJC Scopus subject areas

  • Pharmacology

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Effect of antiarrhythmic drugs, TTX, and 4-aminopyridine on repetitive electrical activity in frog skeletal muscle. / Nánási, P.; Dankó, Miklós; Lathrop, David A.

In: General Pharmacology, Vol. 21, No. 4, 1990, p. 563-567.

Research output: Contribution to journalArticle

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AB - 1. Conventional microelectrode techniques were used to study the effects of antiarrhythmic drugs (quinidine, 2-20 μM; lidocaine, 5-50 μM; verapamil, 2-20 μM), 4-aminopyridine (4-AP, 50-100 μM), and tetrodotoxin (TTX, 1.5-6 nM) on repetitive electrical discharges induced in the muscle membrane in the presence of 1 μM cevadine. 2. Antiarrhythmic drugs and 4-AP produced progressive reduction of the maximum upstroke velocity (V+ max) of the discharges, while the cycle length was prolonged by each drug except 4-AP. 3. The efficacy in depression of V+ max and prolongation of cycle length was not proportional in the case of individual drugs. 4. A simple model of the repetitive activity incorporating drug-effects was presented. The cevadine-modified Na+ channels could be blocked by antiarrhythmic agents, however, the efficacy of these drugs on the normal and cevadine-modified Na+ channels were found to be different.

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