Intralaryngeal CO2 reflexly decreases ventilation and increases upper airway muscle activity. Topical anaesthesia of the laryngeal mucosa or cutting the superior laryngeal nerves (SLNs) abolishes these reflexes, indicating that the receptors responsible are superficially located and that their afferent fibres are in the SLN. Intralaryngeal CO2 affects the activity of receptors recorded from the SLN. An isolated, luminally perfused laryngeal preparation was developed in anaesthetized, paralysed cats in order to compare the effects of solutions with varying levels of pH and PCO2 on pressure‐sensitive laryngeal receptor activity. Since the pH of tracheal surface fluid is reported to be approximately 7.0, two neutral (pH 7.4 and 7.0) and two acidic (pH 6.8 and 6.3) solutions were used. Compared with neutral acapnic control solutions, neutral hypercapnic (PCO2 64 mmHg) solutions either excited or inhibited the discharge of 113 out of 211 pressure‐sensitive SLN afferents. In 24 receptors, the effects of hypercapnic solutions with either neutral or acidic pH were similar in both direction and magnitude. In 50 receptors affected by neutral hypercapnic solutions, acidic acapnic solutions had no effect on 66 % of units and significantly smaller effects in the remaining units. In 17 receptors, the effects of neutral solutions with a PCO2 of 35 mmHg were significantly less than for neutral solution with a PCO2 of 64 mmHg. These results show that the effects of CO2 on laryngeal pressure‐sensitive receptors are independent of the pH of the perfusing media, and suggest that acidification of the receptor cell or its microenvironment is the main mechanism of CO2 chemoreception.

The effects of carbonic anhydrase inhibition on the responsiveness to CO 2 of pressure-sensitive laryngeal receptors were examined in anaesthetised, paralysed cats. Laryngeal CO 2 -sensitive receptors from the superior laryngeal nerve were selected by their responsiveness to intralaryngeal pressure and to perfusion of solution equilibrated with 9 % CO 2 . The carbonic anhydrase inhibitor, methazolamide, when given intralaryngeally at 10 _4 M, diminished or abolished the responses to the CO 2 -equilibrated solution in four of six pressure-sensitive receptors. Histochemical staining for carbonic anhydrase activity showed that the larynges perfused with methazolamide had diminished carbonic anhydrase activity, especially on the superficial layers of surface epithelium. Compared to untreated controls, when given intravenously (50 mg kg