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

Naunyn-Schmiedeberg's Archives of Pharmacology
J KoleyB N Koley

Abstract

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.

References

Apr 1, 1970·European Journal of Pharmacology·B Bhagat
Nov 1, 1974·The Journal of Physiology·R A Chapman, D J Miller
Nov 1, 1963·The American Journal of Physiology·W G Nayler
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Oct 1, 1984·British Journal of Pharmacology·B KoleyJ K Saha

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Citations

Mar 1, 1991·Alcohol·O R CarrylR G Carpentier
Apr 12, 2005·Journal of Cardiovascular Pharmacology·Salma Toma HannaRui Wang
Jun 14, 2000·American Journal of Physiology. Heart and Circulatory Physiology·M YashimaH S Karagueuzian
Oct 17, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Hideki HayashiHrayr S Karagueuzian

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