【摘要】 目的探讨蛋白激酶C(PKC)、蛋白激酶A(PKA)信号转导途经及血管内皮完整性在15-羟基二十碳四烯酸(15-HETE)收缩肺动脉中的作用。方法采用组织浴槽血管环法与PKC、PKA抑制剂以及除去血管内皮细胞相结合的方法。结果用6·8mmol·L-1hypericin阻断PKC途径可使15-HETE收缩缺氧大鼠肺动脉量效曲线右移(P<0·01);用0·112mmol·L-1KT5720阻断PKA途径使15-HETE收缩缺氧大鼠肺动脉量效曲线右移不明显;除去血管内皮细胞可降低对照组和缺氧组肺动脉血管环对15-HETE的反应性。结论15-HETE收缩肺动脉的作用和PKC信号转导系统以及血管内皮细胞的完整性有关。更多还原

【Abstract】 Aim To study the roles of protein kinase A (PKA), protein kinase C (PKC) signal transduction pathway and endothelium (intact or denuded) on 15-hydroxyeicosatetraenoic acid (15-HETE) induced pulmonary vasoconstriction. Methods PKA and PKC inhibitors combined with tension measurements on either endothelium-intact or denuded pulmonary artery (PA) rings were employed. Results Both inhibitions of PKC with 6.8 mmol·L~ -1 hypericin and PKA with 0.112 mmol·L~ -1 KT5720 shifted the dose-response curve of 15-HETE induced pulmonary vasoconstriction to the right, and more powerful inhibition was observed with PKC inhibitor (P<0.01). Denuding endothelia decreased the response of PA ring to 15-HETE in both normoxic and hypoxic PA rings (P<0.05, P<0.01, respectively). Conclusion PKC signal transduction pathway and endothelium-intact are involved in 15-HETE induced rat pulmonary vasoconstriction.更多还原