Laryngeal CO2 receptors: influence of systemic PCO2 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 PCO2 values and before and after carbonic anhydrase inhibition in anesthetized, paralyzed, ventilated cats. Carbonic anhydrase was inhibited, locally, by perfusing the 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 rate in response to 10% intralaryngeal CO2, whereas 3 increased their discharge in response to intralaryngeal CO2. The majority of these receptors also increased their discharge rate in response to positive laryngeal pressure. Neither increased nor decreased systemic PCO2 influenced the receptors' baseline discharge rate or their response to intralaryngeal CO2. Topical inhibition of carbonic anhydrase did not consistently alter the maximal inhibitory response to CO2 or the initial rate of change of receptor activity. On the other hand, intravenous injections 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 laryngeal receptors that are sensitive to intralaryngeal CO2 are not responsive to changes in systemic PCO2. The carbonic anhydrase inhibition experiments show that this enzyme plays an important role in the ability of these receptors to detect both transient and steady-state changes in intralaryngeal CO2.