Acute inhalation of airborne
pollutants alters cardiovascular function and evidence suggests that
pollutant-induced activation of airway sensory nerves via the gating of
ion channels is critical to these systemic responses. Here, we have investigated the effect of
capsaicin [transient receptor potential (TRP) vanilloid 1 (TRPV1) agonist],
AITC [TRP
ankyrin 1 (TRPA1) agonist], and
ATP (P2X2/3 agonist) on bronchopulmonary sensory activity and cardiovascular responses of conscious Sprague-Dawley (SD) rats. Single fiber recordings show that
allyl isothiocyanate (
AITC) and
capsaicin selectively activate C fibers, whereas subpopulations of both A and C fibers are activated by stimulation of P2X2/3 receptors. Inhalation of the agonists by conscious rats caused significant
bradycardia, atrioventricular (
AV) block, and prolonged PR intervals, although
ATP-induced responses were lesser than those evoked by
AITC or
capsaicin. Responses to
AITC were inhibited by the TRP channel blocker
ruthenium red and the
muscarinic antagonist atropine.
AITC inhalation also caused a biphasic blood pressure response: a brief hypertensive phase followed by a hypotensive phase.
Atropine accentuated the hypertensive phase, while preventing the
hypotension.
AITC-evoked
bradycardia was not abolished by
terazosin, the α1-adrenoceptor inhibitor, which prevented the hypertensive response.
Anesthetics had profound effects on
AITC-evoked
bradycardia and
AV block, which was abolished by
urethane,
ketamine, and
isoflurane. Nevertheless,
AITC inhalation caused
bradycardia and
AV block in paralyzed and ventilated rats following precollicular decerebration. In conclusion, we provide evidence that activation of
ion channels expressed on nociceptive airway sensory nerves causes significant cardiovascular effects in conscious SD rats via reflex modulation of the autonomic nervous system.