The role of calcium channel in the effect of nicotine on contractility in isolated toad ventricle

The mechanism of the positive inotropic effect produced by nicotine (6.2 X 10(-5) mol/l to 4.9 X 10(-4) mol/l) on electrically driven toad ventricles was investigated. The response to nicotine was not affected by 6-hydroxydopamine pretreatment, bretylium (2.4 X 10(-4) mol/l) exposure or tyramine tac...

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Bibliographic Details
Published in:Naunyn-Schmiedeberg's archives of pharmacology 1987, Vol.335 (1), p.86-90
Main Authors: KOLEY, J, SAHA, J. K, KOLEY, B
Format: Article
Language:English
Subjects:
Action Potentials - drug effects
Animals
Biological and medical sciences
Bretylium Compounds - pharmacology
Bufo melanostictus
Bufonidae
calcium
Calcium Channel Blockers - pharmacology
Cholinergic system
Hydroxydopamines - pharmacology
In Vitro Techniques
Ion Channels - physiology
Isoproterenol - pharmacology
Medical sciences
Myocardial Contraction - drug effects
Neuropharmacology
Neurotransmitters. Neurotransmission. Receptors
nicotine
Nicotine - pharmacology
Oxidopamine
Pharmacology. Drug treatments
Tyramine - pharmacology
ventricle
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Summary:The mechanism of the positive inotropic effect produced by nicotine (6.2 X 10(-5) mol/l to 4.9 X 10(-4) mol/l) on electrically driven toad ventricles was investigated. The response to nicotine was not affected by 6-hydroxydopamine pretreatment, bretylium (2.4 X 10(-4) mol/l) exposure or tyramine tachyphylaxis. Following desensitisation by isoprenaline (4.2 X 10(-6) mol/l) of the beta-adrenoceptor in the ventricles, the response to nicotine was no affected. However, the response was antagonised by ethylene diamine tetraethyl acetate (2.3 X 10(-4) mol/l), verapamil (0.4 X 10(-5) mol/l) or calcium-free Ringer. Nicotine prolonged the action potential duration and enhanced the force of contraction. Nicotine induced slow action potentials in partially depolarized (in high potassium solution) ventricles and this was antagonised by verapamil (0.4 X 10(-5) mol/l). These results suggest that the effects of nicotine are mediated by a direct interaction with the Ca2+ channels at the cell surface.
ISSN:0028-1298
1432-1912
DOI:10.1007/BF00165041