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HIGHLIGHTED TOPICS
Airway Hyperresponsiveness: From Molecules to
Bedside
Departments of 1Physiology and 2Medicine, University of Kentucky Medical Center, Lexington, Kentucky 40536
Submitted 31 January 2003 ; accepted in final form 12 May 2003
Compelling clinical evidence implicates the potential role of adenosine in
development of airway hyperresponsiveness and suggests involvement of
pulmonary sensory receptors. This study was carried out to determine the
effect of a low dose of adenosine infusion on sensitivity of pulmonary C-fiber
afferents in anesthetized open-chest rats. Infusion of adenosine (40 µg
· kg-1 · min-1 iv
for 90 s) mildly elevated baseline activity of pulmonary C fibers. However,
during adenosine infusion, pulmonary C-fiber responses to chemical stimulants
and lung inflation (30 cmH2O tracheal pressure) were markedly
potentiated; e.g., the response to right atrial injection of capsaicin (0.25
or 0.5 µg/kg) was increased by more than fivefold (change in fiber activity
= 2.64 ± 0.67 and 16.27 ± 3.11 impulses/s at control and during
adenosine infusion, n = 13, P < 0.05), and this enhanced
response returned to control in 
10 min. The potentiating effect of
adenosine infusion was completely blocked by pretreatment with
8-cyclopentyl-1,3-dipropylxanthine (100 µg/kg), a selective antagonist of
the adenosine A1 receptor, but was not affected by
3,7-dimethyl-1-propargylxanthine (1 mg/kg), an A2-receptor
antagonist, or
3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(±)-dihydropyridine-3,5-dicarboxylate
(2 mg/kg), an A3-receptor antagonist. This potentiating effect was
also mimicked by N6-cyclopentyladenosine (0.25
µg·kg-1·min-1 for
90 s), a selective agonist of the adenosine A1 receptor. In
conclusion, our results showed that infusion of adenosine significantly
elevated the sensitivity of pulmonary C-fiber afferents in rat lungs and that
this potentiating effect is likely mediated through activation of the
adenosine A1 receptor.
airway hyperresponsiveness; dyspnea; lung afferents; adenosine receptor; chemical irritants
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