ABSTRACT: Inhalation of noxious irritants/
pollutants activates airway nociceptive afferents resulting in reflex
bradycardia in healthy animals. Nevertheless, noxious
pollutants evoke sympathoexcitation (
tachycardia,
hypertension) in
cardiovascular disease patients. We hypothesize that
cardiovascular disease alters nociceptive pulmonary-cardiac reflexes. Here, we studied reflex responses to irritants in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive (SH) rats. Inhaled
allyl isothiocyanate (
AITC) evoked
atropine-sensitive
bradycardia with atrial-ventricular (
AV) block in conscious WKY rats, thus indicating a parasympathetic reflex. Conversely, inhaled
AITC in conscious SH rats evoked complex brady-
tachycardia with both
AV block and
premature ventricular contractions (PVCs).
Atropine abolished the
bradycardia and
AV block, but the
atropine-insensitive
tachycardia and PVCs were abolished by the β1 -
adrenoceptor antagonist
atenolol. The aberrant
AITC-evoked reflex in SH rats was not reduced by acute blood pressure reduction by
captopril. Surprisingly, intravenous
AITC only evoked
bradycardia in conscious SH and WKY rats. Furthermore, anaesthesia reduced the cardiac reflexes evoked by inhaled but not injected
AITC. Nevertheless, anaesthesia had little effect on
AITC-evoked respiratory reflexes. Such data suggest distinct differences in nociceptive reflex pathways dependent on
cardiovascular disease, administration route and downstream effector.
AITC-evoked
tachycardia in decerebrate SH rats was abolished by
vagotomy. Finally, there was no difference in the cardiac responses of WKY and SH rats to vagal efferent electrical stimulation. Our data suggest that
AITC inhalation in SH rats evokes de novo
adrenergic reflexes following vagal afferent activation. This aberrant reflex is independent of steady state
hypertension and is not evoked by intravenous
AITC. We conclude that pre-existing
hypertension aberrantly shifts nociceptive pulmonary-cardiac reflexes towards sympathoexcitation.