Abstract
The stimulation of rapidly adapting receptors (RARs) in the lungs evoked by cigarette smoke consists of an initial and either a type I or a type II delayed response (Kou and Lee, J. Appl. Physiol. 68: 1203, 1990). In the type I response, receptor activity increased during expirations and exhibited a prominent cardiac modulation, whereas in the type II response, receptor discharge reached its peak during inspiration at peak transpulmonary pressure. To investigate the mechanisms of this stimulation, we recorded the vagal afferent activity arising from 39 RARs and delivered a single breath (120 ml) of cigarette smoke in 15 anesthetized, open-chest and artificially ventilated dogs. Studies were repeated after a pretreatment with aerosolized hexamethonium (3-8 breaths, 10%), aerosolized isoproterenol (12-15 breaths, 2%), or after the cardiac impact on the lung had been minimized by elevating the apex of the heart. The initial response of RARs was totally abolished by hexamethonium but was not affected by isoproterenol. The increase of total lung resistance induced by cigarette smoke and the concomitant type II delayed response of RARs were both abolished by isoproterenol. The type I delayed response of RARs was eliminated or largely attenuated after the apex of the heart had been elevated. Based upon these results, we conclude that a direct effect of nicotine on these receptors may be responsible for the immediate stimulation while the systemic effects of absorbed nicotine may play a part in evoking the delayed stimulation.
Original language | English |
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Pages (from-to) | 61-75 |
Number of pages | 15 |
Journal | Respiration Physiology |
Volume | 83 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1991 |
Bibliographical note
Funding Information:Acknowledgements. The authors wish to thank Dr. Donald Frazier for interest in this study and for allowing the experiment to be carried out in his laboratory. The authors are grateful to Cecil Woolfolk for technical assistance and John Turbek for the statistical analysis of data. This study was supported by University of Kentucky Tobacco and Health Research Institute Grant 41066 and by National Heart, Lung and Blood Institute Program Project Grant HL-40369.
Funding
Acknowledgements. The authors wish to thank Dr. Donald Frazier for interest in this study and for allowing the experiment to be carried out in his laboratory. The authors are grateful to Cecil Woolfolk for technical assistance and John Turbek for the statistical analysis of data. This study was supported by University of Kentucky Tobacco and Health Research Institute Grant 41066 and by National Heart, Lung and Blood Institute Program Project Grant HL-40369.
Funders | Funder number |
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Tobacco and Health Research Institute of the University of Kentucky | 41066 |
National Heart, Lung, and Blood Institute (NHLBI) | P01HL040369 |
Keywords
- Animal, dog
- Bronchoconstriction, and cigarette smoke, and lung receptors
- Drugs, isoproterenol, hexamethonium
- Lung receptors, irritant, rapidly adapting, response to cigarette smoke
- Nicotine
ASJC Scopus subject areas
- Physiology
- Pulmonary and Respiratory Medicine