S. Matsumoto et al., INHIBITORY MECHANISM OF CO2 INHALATION ON SLOWLY ADAPTING PULMONARY STRETCH RECEPTORS IN THE ANESTHETIZED RABBIT, The Journal of pharmacology and experimental therapeutics, 279(1), 1996, pp. 402-409
The inhibitory effects of CO2 on slowly adapting pulmonary stretch rec
eptors (SARs) were studied before and after administration of acetazol
amide, a carbonic anhydrase inhibitor, or nifedipine, a calcium channe
l blocker, in anesthetized, artificially ventilated rabbits after vagu
s nerve section. CO2 inhalation (maximal tracheal CO2 concentration ra
nging from 7.2% to 9.5%) for approximately 60 sec decreased the recept
or activity during both inflation and deflation. The magnitude of decr
eased receptor activity during deflation became more pronounced than t
hat seen during inflation. Acetazolamide treatment (20 mg/kg) diminish
ed the inhibitory responses of slowly adapting pulmonary stretch recep
tors to CO2 inhalation, which were not significantly influenced by pre
treatment with nifedipine (1 mg/kg). Furthermore, CO2 inhalation befor
e and after vagal denervation had no effect on total lung resistance a
nd dynamic lung compliance, in another series of experiments, the stai
ning to determine the presence of carbonic anhydrase enzymatic reactio
n was not found in the smooth muscle of either extrapulmonary or intra
pulmonary bronchi. These results suggest that CO2-induced inhibition o
f slowly adapting pulmonary stretch receptors is not related to the ch
ange in bronchomotor tone.