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2-Nitro-1-phenyl-1-propanol (NPP) is a nitro alcohol with vasodilator activity in the rat aorta. The present study investigated the vasodilator properties of NPP in small vessels of the mesenteric bed, which, contrary to the aorta, contains resistance vessels. Using myography, isometric contractions were recorded in rings of second- and third-order branches from the rat mesenteric artery. NPP relaxed mesenteric ring preparations that were contracted with phenylephrine, U-46619, and KCl (40 mM), resulting in significantly different EC 50 values (0.41 μM [0.31–0.55 μM], 0.16 μM [0.10–0.24 μM], and 4.50 μM [1.86–10.81 μM], respectively). NPP-induced vasodilation decreased as the extracellular K + concentration increased. The pharmacological blockade of K + channels with tetraethylammonium, BaCl 2 , CsCl, and apamin also blunted NPP-induced vasorelaxation. In contrast, NPP-induced vasodilation was resistant to indomethacin, L-N G -nitroarginine methyl ester ( L -NAME), and endothelium removal, indicating that neither prostaglandins nor the endothelial release of nitric oxide is involved in the relaxant effects of NPP. Conversely, 1 H -[1,2,4]oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ), cis- N -(2-phenylcyclopentyl)-azacyclotridec-1-en-2-amine hydrochloride (MDL-12,330 A), and H-89 reduced NPP-induced vasodilation. Under Ca 2+ -free conditions, NPP did not alter transient contractions that were evoked by caffeine, but it reduced transient contractions that were evoked by phenylephrine. In mesenteric rings that were loaded with the fluorescent Ca 2+ indicator Fluo-4 AM and stimulated with phenylephrine, NPP blunted both contractions and fluorescence signals that were related to cytosolic Ca 2+ levels. In conclusion, the vasodilatory actions NPP on mesenteric vessel resistance involved the participation of cyclic nucleotides and the opening of K + channels. [ABSTRACT FROM AUTHOR]

β-Citronellol is a monoterpene found in the essential oil of various plants with antihypertensive properties. In fact, β-citronellol possesses hypotensive actions due to its vasodilator abilities. Here we aimed to show that β-citronellol recruits airway sensory neural circuitry to evoke cardiorespiratory effects. In anesthetized rats, intravenous injection of β-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 β-citronellol effects. P1 persisted after pretreatment with capsazepine, ondansetron, HC-030031 or suramin. Suramin abolished P2 of apnea. In awake rats, β-citronellol induced biphasic hypotension and bradycardia being P1 abolished by methylatropine. In vitro , β-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 β-citronellol. The transduction mechanism in P1 seems not to involve the activation of transient receptor potential vanilloid subtype 1 (TRPV 1 ), transient receptor potential ankyrin subtype 1 (TRPA 1 ), purinergic (P2X) or 5-HT 3 receptors located on airways sensory nerves. P2 of hypotension and bradycardia seems resulting from a cardioinhibitory and vasodilatory effect of β-citronellol and the apnea from a purinergic signaling. [ABSTRACT FROM AUTHOR]

Abstract: Previously, it was shown that intravenous (i.v.) treatment with the essential oil of Aniba canelilla (EOAC) elicited a hypotensive response that is due to active vascular relaxation rather than to the withdrawal of sympathetic tone. The present study investigated mechanisms underlying the cardiovascular responses to 1-nitro-2-phenylethane, the main constituent of the EOAC. In pentobarbital-anesthetized normotensive rats, 1-nitro-2-phenylethane (1–10mg/kg, i.v.) elicited dose-dependent hypotensive and bradycardiac effects which were characterized in two periods (phases 1 and 2). The first rapid component (phase 1) evoked by 1-nitro-2-phenylethane (10mg/kg) was fully abolished by bilateral vagotomy, perineural treatment of both cervical vagus nerves with capsaicin (250µg/ml) and was absent after left ventricle injection. However, pretreatment with capsazepine (1mg/kg, i.v.) or ondansetron (30µg/kg, i.v.) did not alter phase 1 of the cardiovascular responses to 1-nitro-2-phenylethane (10mg/kg, i.v.). In conscious rats, 1-nitro-2-phenylethane (1–10mg/kg, i.v.) evoked rapid hypotensive and bradycardiac (phase 1) effects that were fully abolished by methylatropine (1mg/kg, i.v.). It is concluded that 1-nitro-2-phenylethane induces a vago-vagal bradycardiac and depressor reflex (phase 1) that apparently results from the stimulation of vagal pulmonary rather than cardiac C-fiber afferents. The transduction mechanism of the 1-nitro-2-phenylethane excitation of C-fiber endings is not fully understood and does not appear to involve activation of either Vanilloid TPRV1 or 5-HT3 receptors. The phase 2 hypotensive response to 1-nitro-2-phenylethane seems to result, at least in part, from a direct vasodilatory effect since 1-nitro-2-phenylethane (1–300µg/ml) induced a concentration-dependent reduction of phenylephrine-induced contraction in rat endothelium-containing aorta preparations. [Copyright &y& Elsevier]