U50488H、哌唑嗪及心得安对去甲肾上腺素诱导心肌肥大的作用比较

目的：观测κ阿片受体激动对去甲肾上腺素诱导心肌肥大的抑制作用,并与哌唑嗪、心得安作用进行比较。方法：结晶紫染色法测心肌细胞增殖程度;Lowry法测心肌细胞蛋白含量;计算机图象分析系统测心肌细胞体积;[3H]-亮氨酸掺入法测心肌细胞蛋白合成。结果：①低血清环境下,NE明显诱导心肌细胞蛋白含量、蛋白合成及体积的增加,但对增殖无影响。②哌唑嗪和心得安单独作用部分抑制NE诱导的心肌肥大;联合作用则完全抑制。③U50488H明显抑制NE诱导的心肌肥大;其抑制程度与哌唑嗪和心得安联合作用类似,明显高于二者单独作用。结论：NE通过激动α1-和β-肾上腺受体途径诱导心肌肥大。κ阿片受体激动显著抑制NE诱导的心肌肥大,这可能与干预α1-AR和β-AR途径有关。

Comparing effects of U50488H,prazosin and/or propranolol on cardiac hypertrophy induced by NE in rat

Objective：To demonstrate the inhibitory effect of κ-opioid receptor activation by U50488H on hypertrophy induced by NE in cultured neonatal rat cardiac myocytes and compare its effect with that of prazosin and propranolol.Methods：The cellular proliferation was determined with crystal violet staining.The protein content was assayed with Lowry＇s method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with [3H]-lencine incorporation method.Results：①NE significantly induced the increase of protein content,[3H]-leucine incorporation and cell size without a concomitant increase in cell number in low serum medium.②These responses were partially suppressed by prazosin or propranolol alone and completely abolished by both in combination.③U50488H significantly inhibited the NE-induced increase of protein content,[3H]-leucine incorporation and cell size.The inhibitory effects of U50488H on NE-induced cardiac hypertrophy were greater than either prazosin or propranolol,but comparable to combination of both.Conclusion：NE,acting via both α1-and β-adrenergic pathway,stimulates myocyte hypertrophy.Stimulating κ-opioid receptor significantly inhibits NE-induced cardiac hypertrophy,which may be related with α1-and β-adrenergic pathway.