The response of slowly adapting airway stretch receptors to nicotine aerosol was studied in the paralyzed, artificially ventilated, anesthetized dog. Single‐unit stretch receptor recordings were made from individual vagus nerve filaments placed on a pair of platinum hook electrodes. Administration of 2% nicotine aerosol for five consecutive breaths caused an increase in both the peak transpulmonary pressure (Ptp) and in the activity of the slowly adapting stretch receptors (SARs). The results suggest that tracheal SARs were more affected than those receptors located distal to the carina. Adminsitration of nicotine aerosols following pretreatment with isoproterenol, a bronchodilator, failed to significantly increase Ptp and, concomitantly, the activity of SARs. Therefore, the stimulatory effect of nicotine on SARs appeared to involve primarily an indirect activation of SARs vianicotine‐induced bronchoconstriction. It is suggested that the activation of SARs may be involved in the reported nicotine‐dependent cigarette smoke‐induced apnea.
|Number of pages||11|
|Journal||Journal of Neuroscience Research|
|State||Published - 1986|
- airway receptors
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience