LARYNGEAL CO2 RECEPTORS - INFLUENCE OF SYSTEMIC P-CO2 AND CARBONIC-ANHYDRASE INHIBITION

Responses of laryngeal receptors selected for their responsiveness to 10% intralaryngeal CO2 were recorded in single fibers of the superior laryngeal nerve at a wide range of systemic P-CO2 values and before an d after carbonic anhydrase inhibition in anesthetized, paralyzed, vent ilated cats. Carbonic anhydrase was inhibited, locally, by perfusing t he upper airways with either acetazolamide or methazolamide (10(-2) M) or systemically, by injecting acetazolamide intravenously (5, 10, or 25 mg/kg). Of the 58 receptors studied, 55 decreased their discharge r ate in response to 10% intralaryngeal CO2, whereas 3 increased their d ischarge in response to intralaryngeal CO2. The majority of these rece ptors also increased their discharge rate in response to positive lary ngeal pressure. Neither increased nor decreased systemic P-CO2 influen ced the receptors' baseline discharge rate or their response to intral aryngeal CO2. Topical inhibition of carbonic anhydrase did not consist ently alter the maximal inhibitory response to CO2 or the initial rate of change of receptor activity. On the other hand, intravenous inject ions of acetazolamide caused, within 30 sec, a consistent attenuation of both the initial rate of change and the maximal inhibitory response to intralaryngeal CO2. These results indicate that the sub-set of lar yngeal receptors that are sensitive to intralaryngeal CO2 are not resp onsive to changes in systemic P-CO2. The carbonic anhydrase inhibition experiments show that this enzyme plays an important role in the abil ity of these receptors to detect both transient and steady-state chang es in intralaryngeal CO2.