L. Hansson et al., INHALED NICOTINE IN HUMANS - EFFECT ON THE RESPIRATORY AND CARDIOVASCULAR SYSTEMS, Journal of applied physiology, 76(6), 1994, pp. 2420-2427
Inhalation of nicotine (0-64 mg/ml) and capsaicin (2 X 10(-6)-2.5 X 10
(-4) M) in 24 healthy nonsmoking subjects produced a concentration-dep
endent cough response. Two subjects coughed to capsaicin but not to ni
cotine. The mean (95% confidence interval) nicotine concentrations cau
sing two and five coughs were 5.5 (3.5-8.7) and 15.8 (10.0-25.1) mg/ml
, respectively, and were reproducible over 3 different days. Capsaicin
inhalation did not alter the response to nicotine and vice versa. Bot
h agents increased respiratory resistance, but the response was more r
apid to capsaicin. Inhalation of nicotine (0-8 mg/ml) over 5 min cause
d increases in heart rate and blood pressure and a decrease in skin te
mperature. Inhaled ipratropium bromide (0.50 mg) had an antitussive ef
fect and also inhibited the nicotine-induced bronchoconstriction, indi
cating a vagally mediated effect. Sodium cromoglycate (0.20 mg) did no
t affect cough or airway resistance changes caused by nicotine. This s
tudy shows that inhaled nicotine produces a concentration-dependent co
ugh and airway obstruction in healthy subjects, probably because of st
imulation of afferent nerve endings in the bronchial mucosa and mediat
ed through parasympathetic cholinergic pathways. Respiratory reflexes
evoked by nicotine are similar to those produced by capsaicin, but it
is unclear whether these reflexes are mediated by the same type of sen
sory nerves.