RESUMO
ß-Citronellol is a monoterpene found in the essential oil of various plants with antihypertensive properties. In fact, ß-citronellol possesses hypotensive actions due to its vasodilator abilities. Here we aimed to show that ß-citronellol recruits airway sensory neural circuitry to evoke cardiorespiratory effects. In anesthetized rats, intravenous injection of ß-citronellol caused biphasic hypotension, bradycardia and apnea. Bilateral vagotomy, perivagal capsaicin treatment or injection into the left ventricle abolished first rapid phase (named P1) but not delayed phase P2 of the ß-citronellol effects. P1 persisted after pretreatment with capsazepine, ondansetron, HC-030031 or suramin. Suramin abolished P2 of apnea. In awake rats, ß-citronellol induced biphasic hypotension and bradycardia being P1 abolished by methylatropine. In vitro, ß-citronellol inhibited spontaneous or electrically-evoked contractions of rat isolated right or left atrium, respectively, and fully relaxed sustained contractions of phenylephrine in mesenteric artery rings. In conclusion, chemosensitive pulmonary vagal afferent fibers appear to mediate the cardiovascular and respiratory effects of ß-citronellol. The transduction mechanism in P1 seems not to involve the activation of transient receptor potential vanilloid subtype 1 (TRPV1), transient receptor potential ankyrin subtype 1 (TRPA1), purinergic (P2X) or 5-HT3 receptors located on airways sensory nerves. P2 of hypotension and bradycardia seems resulting from a cardioinhibitory and vasodilatory effect of ß-citronellol and the apnea from a purinergic signaling.