Vol. 290, Issue 3, 974-979, September 1999

Effects of Potassium Channel Blockers on CO₂-Induced Slowly Adapting Pulmonary Stretch Receptor Inhibition

Shigeji Matsumoto, Toshiaki Takahashi, Takeshi Tanimoto, Chikako Saiki and Mamoru Takeda

Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, Tokyo, Japan

In anesthetized, artificially ventilated rabbits with vagus nerve section, inhalation of CO₂ gas mixtures (tracheal CO₂ 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. CO₂ 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 CO₂ 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 CO₂ inhalation. These results suggest that the inhibitory mechanism of CO₂ inhalation on SARs may be involved in the activation of 4-aminopyridine-sensitive K⁺ channels in the nerve terminals of SARs.