Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Eur J Pharmacol. 2010 Jul 25;638(1-3):90-8. doi: 10.1016/j.ejphar.2010.03.060. Epub 2010 Apr 18.
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 (250 microg/ml) and was absent after left ventricle injection. However, pretreatment with capsazepine (1mg/kg, i.v.) or ondansetron (30 microg/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 TPRV(1) or 5-HT(3) 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 (1-300 microg/ml) induced a concentration-dependent reduction of phenylephrine-induced contraction in rat endothelium-containing aorta preparations.
先前的研究表明，静脉内（i.v.）给予 Aniba canelilla 精油（EOAC）可引起降压反应，这是由于血管主动松弛而不是交感神经张力的撤回所致。本研究探讨了 1-硝基-2-苯乙烷对心血管反应的机制，1-硝基-2-苯乙烷是 EOAC 的主要成分。在戊巴比妥钠麻醉的正常血压大鼠中，1-硝基-2-苯乙烷（1-10mg/kg，i.v.）引起剂量依赖性的降压和心动过缓作用，其特征在于两个时期（阶段 1 和 2）。1-硝基-2-苯乙烷（10mg/kg）引起的第一个快速成分（阶段 1）被双侧迷走神经切断术完全消除，双侧颈迷走神经的神经周用辣椒素（250μg/ml）处理，左心室注射后消失。然而，用辣椒素预处理（1mg/kg，i.v.）或昂丹司琼（30μg/kg，i.v.）并不改变 1-硝基-2-苯乙烷（10mg/kg，i.v.）对心血管反应的阶段 1。在清醒大鼠中，1-硝基-2-苯乙烷（1-10mg/kg，i.v.）引起快速降压和心动过缓（阶段 1）作用，这些作用被甲硫酸阿托品（1mg/kg，i.v.）完全消除。结论是，1-硝基-2-苯乙烷诱导的迷走神经-迷走神经心动过缓和降压反射（阶段 1）显然是由于刺激肺而非心脏 C 纤维传入纤维引起的。1-硝基-2-苯乙烷兴奋 C 纤维末梢的转导机制尚不完全清楚，似乎不涉及激活香草素 TRPV(1)或 5-HT(3)受体。1-硝基-2-苯乙烷的阶段 2 降压反应似乎至少部分是由于直接的血管扩张作用所致，因为 1-硝基-2-苯乙烷（1-300μg/ml）诱导了对苯肾上腺素诱导的大鼠内皮包含主动脉制剂收缩的浓度依赖性降低。
