Noradrenaline-ATP corelease and cotransmission following activation of nicotine receptors at postganglionic sympathetic axons
In rabbit mesenteric arteries, nicotine-evoked vasoconstrictor responses were markedly reduced by prazosin, slightly reduced after desen- sitization by α, β-methylene ATP, and abolished by combined treatment with prazosin and α, β-methylene ATP. In guinea-pig vasa deferentia preincubated with [3H]noradrenaline, nicotine elicited contractions as well as an overflow of tritium and of ATP. The contractions were greatly reduced by prazosin and abolished after additional desensitization by α, β-methylene ATP. The nicotine- induced overflow of tritium was not changed by either treatment. The overflow of ATP was decreased by prazosin but not diminished further after additional desensitization by α, β-methylene ATP. Activation of prejunctional nicotine receptors elicits a corelease of noradrenaline and ATP which leads to eotransmission in both tissues.
KeywordsSympathetic Nerve Stimulation Ileocolic Artery Sympathetic Axon Exogenous Noradrenaline Postganglionic Sympathetic Nerve
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