1. Intravenous administration of adenosine (Ado) to patients can cause dyspnoea, chest discomfort and bronchoconstriction. To assess the role of vagal pulmonary C fibres in evoking these adverse reactions, the effect of Ado on single pulmonary C fibres was studied in anaesthetized and artificially ventilated rats. 2. Right-atrial injection of Ado (320 μg kg-1) activated 68% (73/107) of pulmonary C fibres; the total number of action potentials during a period of 15 s increased from a baseline of 0.2 ± 0.1 impulses to a peak of 16.4 ± 2.6 impulses (P < 0.01, n = 107) after Ado. Inosine, the metabolite of Ado, did not activate any of eleven C fibres tested in six rats. Furthermore, C fibres were activated only by right-atrial and not by left-ventricular injection of the same dose of Ado. 3. Unlike the immediate and transient stimulation of C fibres by capsaicin, the C fibre stimulation by Ado had a latency of 6.5 ± 0.3 s (range 3-18 s) and lasted longer. 4. The stimulation of C fibres by Ado was significantly attenuated by pretreatment with aminophylline, a non-selective Ado receptor antagonist, was completely prevented by 1,3-dipropyl-8-cyclopentylxanthine, an Ado A1 receptor antagonist, but was unaffected by 3,7-dimethy-1-propargylxanthine, an A2 receptor antagonist. None of these Ado receptor antagonists prevented capsaicin-induced C fibre stimulation. 5. In conclusion, Ado stimulates pulmonary C fibre terminals through an activation of A1 receptors. The stimulation of pulmonary C fibres may play an important role in Ado-induced adverse respiratory effects.
|Number of pages||10|
|Journal||Journal of Physiology|
|State||Published - Apr 1 1998|
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