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Demonstrates that nicotine enhances adrenergic neuroeffector transmission and increases noradrenaline release in isolated rabbit ear arteries, indicating nicotinic receptor-mediated facilitation.
The effects of nicotine were studied on perfusion pressure and vasoconstrictor responses to sympathetic nerve stimulation in the isolated ear artery of the rabbit. Infusions of nicotine (50 micro M) produced a transient increase in perfusion pressure and potentiated responses to nerve stimulation; these effects of nicotine were unaffected by atropine (0.3 micro M) and abolished or significantly reduced respectively by hexamethonium (300 micro M) or mecamylamine (1 micro M). In experiments with ear arteries previously labelled with [3H] noradrenaline an infusion of nicotine (50 micro M) produced a transient increase in tritium efflux and the potentiation of responses to nerve stimulation in the presence of nicotine was accompanied by a statistically significant increase in stimulation-induced tritium efflux; these effects of nicotine were abolished by hexamethonium (300 micro M) or mecamylamine (1 micro M).
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Sarantos-Laska et al. (1980) studied this question.
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