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MECHANISM OF NICOTINE‐INDUCED RELEASE OF NORADRENALINE FROM ADRENERGIC NERVE ENDINGS
Author(s) -
JAYASUNDAR S.,
VOHRA M.M.
Publication year - 1977
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1977.tb08403.x
Subject(s) - free nerve ending , nicotine , adrenergic , norepinephrine , chemistry , neuroscience , mechanism (biology) , medicine , pharmacology , endocrinology , biology , dopamine , receptor , philosophy , epistemology
1 A study of the mechanism of release of [ 3 H]‐noradrenaline ([ 3 H]‐NA) by nicotine from isolated vas deferens of the rat was made using incubation media of different ionic composition. 2 Nicotine (20 μg/ml)‐induced release of [ 3 H]‐NA was significantly potentiated in K + ‐free Krebs solution as compared to that in normal Krebs‐Ringer solution. 3 Nicotine‐induced release of [ 3 H]‐NA was significantly reduced in Na + ‐deficient Krebs solution (containing only 11 mM Na + ) and was abolished in Na + ‐free Krebs solution. 4 In totally depolarized tissues, nicotine failed to cause an outflow of [ 3 H]‐NA but Ca 2+ (5 mM) did so. 5 Nicotine required the presence of Ca 2+ in the incubation medium to cause release of [ 3 H]‐NA from adrenergic nerve terminals, the magnitude of release being dependent upon the concentration of Ca 2+ . 6 Nicotine‐induced release of [ 3 H]‐NA was demonstrated in high Ca 2 +, Na + ‐free Krebs solution in which all Na + had been replaced with Ca 2+ . 7 It is concluded that nicotine increases the membrane permeability to both Na + and Ca 2+ . It is also suggested that the increase in permeability to Ca 2+ alone is not sufficient but a local depolarizing action of nicotine is necessary to cause release of noradrenaline from adrenergic nerve endings.