Mechanism of the ropivacaine-induced increase in intracellular Ca2+ concentration in rat aortic smooth muscle

作者：Tokinaga Y^*; Ogawa K; Yu J; Kuriyama T; Minonishi T; Hatano Y

来源：Acta Anaesthesiologica Scandinavica, 2007, 51(9): 1155-1160.

DOI：10.1111/j.1399-6576.2007.01390.x

• anesthetic
• calcium
• muscle contraction
• ropivacaine

Background: Ropivacaine is a long-acting local anesthetic with low cardiac toxicity that induces vasoconstriction in vitro and in vivo. Vascular smooth muscle tone is regulated by changes in both intracellular Ca2+ concentration ([Ca2+](i)) and myofilament Ca2+ sensitivity. Therefore, the aim of this study was to examine the mechanism underlying the increase in [Ca2+](i) in ropivacaine-induced vascular contraction.
Methods: Ropivacaine-induced contractile responses and changes in [Ca2+](i) were examined using an isometric force transducer and a fluorometer, respectively.
Results: Ropivacaine induced a biphasic, concentration-dependent change in [Ca2+](i) and contractile response in rat aortic smooth muscles: an increase in [Ca2+](i) occurred at lower ropivacaine concentrations (3 x 10(-5) to 3 x 10(-4) M) and a decrease was observed at higher concentrations (10(-3) to 3 x 10(-3) M). Contraction and the [Ca2+](i) increase induced by ropivacaine were attenuated significantly by a voltage-dependent Ca2+ channel antagonist, an inositol 1,4,5-triphosphate receptor antagonist and Ca2+-free solution (P < 0.01, n= 6).
Conclusion: Ropivacaine-induced contraction of rat aortic smooth muscle is, in part, regulated by Ca2+ influx from the extracellular space and Ca2+ release from the sarcoplasmic reticulum.

• 出版日期2007-10
• 单位山东大学