The histamine H3-agonist (R)-α-methylhistamine (α-MeHA) caused a dose-dependent inhibition of vagally-mediated contraction of a guinea-pig tracheal tube preparation but did not alter tracheal contraction induced by exogenously-applied acetylcholine. Blockade of H1- and H2-histamine receptors, and α- and β-adrenoceptors failed to prevent the inhibitory effect of α-MeHA, whereas the specific H3-antagonist thioperamide prevented the effect of α-MeHA on tracheal contraction. In the presence of H1- and H2-receptor antagonists, histamine also inhibited vagally-mediated tracheal contraction. The inhibitory effect of α-MeHA was greater with preganglionic (vagus nerve) stimulation than with postganglionic stimulation by electrical field stimulation, suggesting that H3-receptors are localized both to cholinergic ganglia and to post-ganglionic nerve-endings. Our results suggest thatl H3-receptors exist on the vagus nerve which modulate cholinergic neurotransmission in the airways.
|Number of pages||3|
|Journal||British Journal of Pharmacology|
|Publication status||Published - 1989|
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