Sensitization of vagal lung C fibers has been postulated to contribute to the development of asthma, but support for this notion is still lacking. We investigated the characteristics and function of pulmonary C fibers (PCFs) in ovalbumin (OVA)-sensitized Brown Norway rats, an established animal model of asthma. Rats were sensitized with intraperitoneal injection of OVA or were treated with saline (control). In study 1 using open-chest and artificially ventilated rats, inhalation of 5% OVA aerosol evoked an augmented increase in total lung resistance (RL) in the OVA-sensitized rats, compared with the control rats. Bilateral vagotomy or subcutaneous pretreatment with a high-dose of capsaicin for blocking of C-fiber function equally attenuated this augmented RL response, suggesting the involvement of PCFs. In study 2 using anesthetized, spontaneously breathing rats, right atrial injection of capsaicin (1 µg/kg; a PCF stimulant) evoked an augmented apneic response in the OVA-sensitized rats, compared with the control rats. In study 3 using open-chest, paralyzed and artificially ventilated rats, the afferent PCF responses to right atrial injection of capsaicin (0.5 and 1.0 µg/kg), phenylbiguanide (8 µg/kg; a PCF stimulant) or adenosine (0.2 mg/kg; a PCF stimulant) were enhanced in the OVA-sensitized rats, compared with the control rats. However, the baseline activities of PCFs and their afferent responses to mechanical stimulation by lung hyperinflation in the OVA-sensitized and control rats were comparable. Our results suggested that OVA-sensitized Brown Norway rats possess sensitized vagal pulmonary C fibers, which may participate in the development of airway hyperreactivity observed in these animals.