Department of Physiology and Pharmacology, Federal University of Ceará, Fortaleza, CE, Brazil.
Department of Health Sciences, Rural Federal University of the Semiarid, Mossoró, RN, Brazil.
Naunyn Schmiedebergs Arch Pharmacol. 2020 Jan;393(1):43-55. doi: 10.1007/s00210-019-01709-z. Epub 2019 Aug 16.
Neryl butyrate is a constituent of volatile oils obtained from aromatic plants. Aliphatic organic compound analogues chemically close to neryl butyrate possess vasodilator properties in rat aorta. To evaluate whether neryl butyrate has relaxing properties, this study tested its effects on isolated rat aorta. Unlike the analogues, neryl butyrate did not show relaxant profile in aortic rings precontracted with phenylephrine, but induced a contraction when it stimulated aortic rings under resting tonus. The contractile effect augmented in endothelium-denuded aortic rings. Treatment of endothelium-intact preparations with the nitric oxide synthase inhibitor L-NAME or the guanylyl cyclase inhibitor ODQ also augmented the contractile effect of neryl butyrate. Such phenomenon was absent in the presence of the cyclooxygenase inhibitor indomethacin. Contractile responses decreased in the presence of verapamil, a L-type Ca channel blocker, or when Ca was removed from the extracellular solution. Antagonists of α-adrenergic receptors (prazosin and yohimbine), but not the thromboxane-prostanoid receptor seratrodast, reversed the contraction induced by neryl butyrate. The α selective antagonist RS-17053 antagonized the neryl butyrate-induced contraction. The contraction caused by neryl butyrate was decreased by inhibiting the phospholipase C or the rho-associated kinase with U-73122 or Y-27632, respectively. Injected intravenously to awake rats, neryl butyrate induced arterial hypotension and bradycardia. Decreased frequency was also present in isolated right atrium preparations. In conclusion, the contractile effects of neryl butyrate were inhibited by α-adrenergic antagonists, indicating the involvement of α-adrenoceptors in the mechanism of action. In vivo, neryl butyrate caused hypotension, suggesting that other systemic influence than vasoconstriction may occur.
丁酸沉香酯是从芳香植物中提取的挥发性油的成分。化学上与丁酸沉香酯接近的脂族有机化合物类似物在大鼠主动脉中具有血管扩张作用。为了评估丁酸沉香酯是否具有松弛特性，本研究测试了其对分离的大鼠主动脉的影响。与类似物不同，丁酸沉香酯在预先用苯肾上腺素收缩的主动脉环中没有显示出松弛特性，而是在静息张力下刺激主动脉环时引起收缩。在去内皮的主动脉环中，收缩作用增强。用一氧化氮合酶抑制剂 L-NAME 或鸟苷酸环化酶抑制剂 ODQ 处理完整内皮的制剂也增强了丁酸沉香酯的收缩作用。在存在环氧化酶抑制剂吲哚美辛的情况下，这种现象不存在。在存在 L 型钙通道阻滞剂维拉帕米或从细胞外溶液中除去 Ca 的情况下，收缩反应减少。α-肾上腺素能受体拮抗剂（哌唑嗪和育亨宾）而非血栓素-前列腺素受体塞拉曲多逆转了丁酸沉香酯引起的收缩。α 选择性拮抗剂 RS-17053 拮抗了丁酸沉香酯诱导的收缩。用 U-73122 或 Y-27632 分别抑制磷脂酶 C 或 rho 相关激酶，可降低丁酸沉香酯引起的收缩。静脉注射到清醒大鼠体内，丁酸沉香酯引起动脉低血压和心动过缓。在分离的右心房制剂中也存在频率降低。总之，丁酸沉香酯的收缩作用被 α-肾上腺素能拮抗剂抑制，表明 α-肾上腺素能受体参与了作用机制。在体内，丁酸沉香酯引起低血压，表明可能发生除血管收缩以外的其他全身影响。
