Activation of dopamine D2-like receptors attenuates pulmonary C-fiber hypersensitivity in rats

You Shuei Lin, Qihai Gu, Lu Yuan Lee

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)


This study was performed to determine whether activation of dopamine D2-like receptors inhibits the hyperresponsiveness of pulmonary C fibers induced by inflammatory mediators such as prostaglandin E2 (PGE2). In anesthetized, open-chest rats, constant infusion of PGE2 (1.5-4.5 μg/kg per minute, 2 minutes) significantly enhanced the C-fiber response to capsaicin injection. At 20 minutes after pretreatment with quinpirole (3 mg/kg, intravenous), a D2-like receptor agonist, the hyperresponsiveness to capsaicin of the same C fibers induced by PGE2 infusion was markedly attenuated, and this inhibitory effect lasted for more than 90 minutes. The effect of quinpirole was dose dependent and was antagonized by pretreatment with domperidone (5 mg/kg, intravenous), a D2-like receptor antagonist, administrated 10 minutes before the quinpirole injection. In a separate series of experiments, C-fiber responses to injections of phenyl biguanide and lactic acid and to constant-pressure lung inflation were augmented by PGE2; these potentiating responses were also significantly reduced by quinpirole. Furthermore, the effect of quinpirole was equally effective in inhibiting the increase in excitability of pulmonary C fibers induced by alveolar hypercapnia or constant infusion of adenosine. In conclusion, these results clearly show that activation of the dopamine D2-like receptors attenuates the hyperresponsiveness of pulmonary C fibers to both chemical stimuli and lung inflation.

Original languageEnglish
Pages (from-to)1096-1101
Number of pages6
JournalAmerican Journal of Respiratory and Critical Care Medicine
Issue number8
Publication statusPublished - Apr 15 2003
Externally publishedYes


  • Inflammation mediators
  • Quinpirole
  • Respiratory hypersensitivity
  • Sensory

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine


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