κ-阿片受体与β1-肾上腺素受体交互作用抑制异丙肾上腺素诱导的心肌肥大

目的: 观察选择性 kappa 阿片受体(kappa opi-oid receptor,κ-OR)与 β 肾上腺素受体(β adrenergicreceptor, β-AR)在心肌细胞肥大方面的交互作用。方法: 以 体 外 培 养 的 乳 鼠 心 肌 细 胞 为 模 型, 10 μmol°L^-1 的异丙肾上腺素(β肾上腺素受体激动剂,β-AR)诱导心肌肥大, 观察 1μmol°L^-1的 U50,488H(κ-OR激动剂,U50)对其作用。进一步探索在100 nmol°L^-1ICI118, 551(β₂ -AR 阻断剂)存在情况下,κ-OR的激活对心肌肥大的作用。用 Lowry's 法测心肌细胞的蛋白质含量;用消化分离法,并利用计算机图象分析系统测心肌 细胞的体积;用³H]leucine 掺入法测定心肌细胞蛋白的合成。结果: 异丙肾上腺素使心肌细胞总蛋白含量、体积、蛋白合成明显增加;1 μmol°L^-1 的 U50, 488H 使 ISO 诱导的心肌细胞总蛋白含量、体积、蛋白合成减少, 这种作用可被选择性 κ-OR阻断剂-nor-BNI(norbinaltorphimine)抑制。在 ICI118, 551 存在的情况下, U50 也能起到减弱 ISO 诱导心肌细胞肥大的作用。结论: U50,488H 通过激活 κ-OR 与β₁ -AR 交互作用抑制 ISO 所诱导的心肌细胞肥大。

Inhibition effects of U50, 488H on hypertrophic myocardial cells induced by isoproterenol

AIM: To observe the inhibition effects of cross-talk between kappa opioid receptor (κ-OR)and β₁ -adrenoceptor (β₁ -AR)on hypertrophic myocardial cells induced by isoproterenol (ISO)in neonatal rats.METHODS: The total protein content was assayed by the meth-od of Lowry's.The cardiomyocytes' volume was mea-sured by computer photograph analysis system and the protein synthesis was assayed with ³H] leucine intake method. RESULTS: ISO enhanced the total protein con-tent, the cardiomyocytes' volume and the protein synthe-sis in myocardial cells.U50, 488H (U50)showed the function inhibited by nor-BNI on reducing the previous mentioned indices induced by ISO.U50 also attenuated the hypertrophy induced by ISO combined with ICI118, 551(β₂ -AR inhibitor).CONCLUSION: κ-OR has a cross-talkwith β₁ -adrenoceptor in ISO-induced myocardial hypertrophy.