Silva-Filho José Couras, Oliveira Nelma Neylanne P M, Arcanjo Daniel D R, Quintans-Júnior Lucindo J, Cavalcanti Sócrates C H, Santos Márcio Roberto V, Oliveira Rita de Cássia M, Oliveira Aldeídia P
Medicinal Plants Research Center, Federal University of Piauí, BrazilDepartament of Physiology, Federal University of Sergipe, Brazil.
Basic Clin Pharmacol Toxicol. 2012 Feb;110(2):171-7. doi: 10.1111/j.1742-7843.2011.00784.x. Epub 2011 Sep 28.
The monoterpene (-)-borneol is present in essential oils of several medicinal plants. The aim of this study was to evaluate (-)-borneol effects on rat thoracic aorta artery rings. The cumulative addition of (-)-borneol (10(-9) -3 × 10(-4) M) on a phenylephrine-induced pre-contraction (10(-6) M) promoted a vasorelaxant effect in a concentration-dependent manner and independent of vascular endothelium. A similar effect was obtained on KCl-induced pre-contractions (80 mM). (-)-Borneol (10(-5) -3 × 10(-4 ) M) inhibited contractions induced by cumulative addition of CaCl2 (10(-6) -3 × 10(-2) M) in depolarizing medium without Ca(2+) in a concentration-dependent manner. On S-(-) Bay K 8644-induced pre-contractions (10(-7) M), (-)-borneol did not induce significant changes compared with KCl-induced pre-contractions. In a Ca(2+) -free medium, (-)-borneol (10(-5) , 10(-4) or 10(-3) M) interfered in calcium mobilization from phenylephrine (10(-6) M)- or caffeine (20 mM)-sensitive intracellular stores. The involvement of K(+) channels was evaluated by tetraethylammonium (3 mM), 4-aminopyridine (1 mM) and glibenclamide (10(-5) M) pre-treatment, and (-)-borneol-induced vasorelaxation was markedly attenuated. Thus, this vasorelaxant effect can probably be attributed to calcium influx blockade through voltage-operated calcium channels (CaV L), calcium mobilization from intracellular stores and potassium channels activation.
单萜（-）-冰片存在于多种药用植物的精油中。本研究旨在评估（-）-冰片对大鼠胸主动脉环的影响。在苯肾上腺素诱导的预收缩（10⁻⁶ M）基础上累积添加（-）-冰片（10⁻⁹ - 3×10⁻⁴ M），可促进血管舒张作用，呈浓度依赖性且与血管内皮无关。在氯化钾诱导的预收缩（80 mM）上也获得了类似效果。（-）-冰片（10⁻⁵ - 3×10⁻⁴ M）在无钙的去极化培养基中，以浓度依赖性方式抑制氯化钙（10⁻⁶ - 3×10⁻² M）累积添加所诱导的收缩。在S-（-）Bay K 8644诱导的预收缩（10⁻⁷ M）上，与氯化钾诱导的预收缩相比，（-）-冰片未引起显著变化。在无钙培养基中，（-）-冰片（10⁻⁵、10⁻⁴或10⁻³ M）干扰了苯肾上腺素（10⁻⁶ M）或咖啡因（20 mM）敏感的细胞内钙库的钙动员。通过四乙铵（3 mM）、4-氨基吡啶（1 mM）和格列本脲（10⁻⁵ M）预处理评估钾通道的参与情况，（-）-冰片诱导的血管舒张明显减弱。因此，这种血管舒张作用可能归因于通过电压门控钙通道（CaV L）的钙内流阻断、细胞内钙库的钙动员以及钾通道的激活。
