Effects of potassium channel blockers on CO2-induced slowly adapting pulmonary stretch receptor inhibition.

In anesthetized, artificially ventilated rabbits with vagus nerve section, inhalation of CO(2) gas mixtures (tracheal CO(2) concentration ranging from 8.0 to 10.2%) for 60 s decreased slowly adapting pulmonary stretch receptor (SAR) activity during both inflation and deflation. The magnitude of decreased receptor activity during deflation had a more pronounced effect than that seen during inflation. CO(2) inhalation did not cause any significant change in tracheal pressure (P(T)) as an index of bronchomotor tone. Intravenous administration of 4-aminopyridine (0. 7 and 2.0 mg/kg i.v.), a K(+) channel blocker, which dose-dependently increased SAR activity during deflation and had no effect on P(T), abolished or attenuated the decrease in SAR activities induced by CO(2) inhalation in a dose-dependent manner. The K(+) channel blocker tetraethylammonium (2.0 and 6.0 mg/kg i.v.) that did not significantly alter either basal SAR discharge or P(T) had no effect on the inhibitory responses of receptor activity to CO(2) inhalation. These results suggest that the inhibitory mechanism of CO(2) inhalation on SARs may be involved in the activation of 4-aminopyridine-sensitive K(+) channels in the nerve terminals of SARs.