Intrapulmonary chemoreceptors (IPC) are CO2-sensitive sensory neurons that innervate the lungs of birds. Current evidence suggests that IPC CO2 response requires carbonic anhydrase (CA) and that pH is the likely cellular determinant of IPC sensory discharge. In this study we test whether CA enzyme is located intra- or extra-cellularly in IPC by quantifying the effect of relatively membrane permeant lacetazolamide) and relatively impermeant (benzolamide) CA inhibitors on IPC response to CO2. Single fiber recordings were made from 9 anesthetized, unidirectionally ventilated Anas platyrhynchos. Inspired CO2 was stepped from 0% to 7% to identify IPC, and then held steady at levels between 1% and 7% to measure steady IPC response to CO2. Without CA inhibition, IPC discharge rate was inversely proportional to inspired PCO2 (slope -8.9 ± 1.0 sec-1.InTorr-1; μ±sem, n = 9). Infusion of 25 mg/kg benzolamide (i.v.) had no significant effect on IPC CO2 sensitivity (slope -8.5±1.4 sec-1.InTorr-1, n = 7), but 25 mg/kg acetazolamide nearly eliminated sensitivity (slope -0.3 ± 1.0 sec-1.InTorr-1, n = 2). High doses of benzolamide (100 mg/kg) decreased CO2 sensitivity to -3.2 ± 0.6 sec-1.InTorr-1, n = 3, but sensitivity remained greater than with 25mg/kg acetazolamide. Our results suggest that an intracellular rather than extracellular carbonic anhydrase catalyzes hydration of CO2 to carbonic acid in IPC, and that intracellular H+ controls IPC discharge rate.
|Original language||English (US)|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology