SUMMARY1. We studied the characteristics of pulmonary sensory receptors whose afferent fibres are in the left vagus nerve of opened-chest rats. The activity of these receptors was recorded during mechanical ventilation approximating eupnoea, as well as during deflation, stepwise inflations and constant-pressure inflations of the lungs. Data were also collected from closed-chest rats and analysed separately.2. Ninety-four per cent of receptors were located in the ipsilateral lung or airways with the remainder in the contralateral lung.3. Not only were slowly adapting receptors (SARs) the most abundant pulmonary receptors but 21 % of them were either exclusively or predominantly active during the deflationary phase of the ventilatory cycle. Deflationary units were found in opened-and closed-chest rats. The average conduction velocity for all fibres innervating SARs averaged 29-7 m s-'. 4. We found rapidly adapting receptors (RARs) to be extremely rare in the rat. Their activity was sparse and irregular. The conduction velocities of fibres innervating RARs averaged 12 3 m s-'.5. Far more abundant than RARs in the remaining population of pulmonary fibres were C fibres. They were observed to have an average conduction velocity of 2-1 m s-1, base-level activity which was irregular and a high pressure threshold of activation and were stimulated by intravenous capsaicin injection.6. Notable differences exist between pulmonary receptors in rats and those reported in other species. The variations include the abundant existence of intrapulmonary SARs with exclusively deflationary modulation and the rarity of RARs. We also encountered C fibres which have not previously been described systematically in the rat.

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Tobacco smoke (TS) exposure induces airway hyperreactivity, particularly in sensitive individuals with asthma. However, the mechanism of this airway hyperreactivity is not well understood. To investigate the relative susceptibility of atopic and nonatopic individuals to TS-induced airway hyperreactivity, we exposed ovalbumin (OA)-sensitized and nonsensitized guinea pigs to TS exposure (5 mg/l air, 30-min exposure, 7 days/wk for 120-156 days). Two similar groups exposed to compressed air served as controls. Airway reactivity was assessed as an increase in enhanced pause (Penh) units using a plethysmograph that allowed free movement of the animals. After 90 days of exposure, airway reactivity increased in OA-TS guinea pigs challenged with capsaicin, bradykinin, and neurokinin A fragment 4--10 aerosols. In addition, substance P content increased in lung perfusate of OA-TS guinea pigs in response to acute TS challenge compared with that of the other groups. Airway hyperirritability was not enhanced by phosphoramidon but was attenuated by a cocktail of neurokinin antagonists, nor was airway hyperreactivity observed after either methacholine or histamine challenge in OA-TS guinea pigs. Chronic TS exposure enhanced neither airway reactivity to histamine or methacholine nor contractility of isolated tracheal rings. In conclusion, chronic TS exposure increased airway reactivity to capsaicin and bradykinin aerosol challenge, and OA-TS guinea pigs were most susceptible to airway dysfunction as the result of exposure to TS compared with the other groups. Increased airway reactivity to capsaicin suggests a mechanism involving neurogenic inflammation, such as increased activation of lung C fibers.