Effects of Potassium Channel Blockers on CO2-Induced Slowly Adapting Pulmonary Stretch Receptor Inhibition
Abstract
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 (PT) 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 PT, 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 PT had no effect on the inhibitory responses of receptor activity to CO2inhalation. 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.
Footnotes
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Send reprint requests to: Dr. Shigeji Matsumoto, Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo 102-8159, Japan.
- Abbreviations:
- SAR
- slowly adapting pulmonary stretch receptor
- PT
- tracheal pressure
- BP
- blood pressure
- MBP
- mean blood pressure
- 4-AP
- 4-aminopyridine
- TEA
- tetraethylammonium
- CA
- carbonic anhydrase
- Ia
- fast transient outward K+ current
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- Received December 28, 1998.
- Accepted April 28, 1999.
- The American Society for Pharmacology and Experimental Therapeutics
