大鼠心肌线粒体L-Arg/NO系统对线粒体Ca^(2+)转运功能的影响

EFFECTS OF MITOCHONDRIAL L-ARGININE/NITRIC OXIDE SYSTEM ON MITOCHONDRIAL Ca^(2+) TRANSPORT IN RAT MYOCARDIUM

目的和方法 :采用大鼠心肌线粒体体外孵育的方法 ,观察线粒体L 精氨酸 一氧化氮系统对线粒体Ca2 +转运功能的影响。结果 :NO生成的底物L Arg (10 - 4 mol L)、外源性NO供体硝普纳 (5× 10 - 7mol L)孵育的线粒体NO-2 的生成量分别高于对照组 6 6 %、89% (P <0 .0 1) ;钙含量较对照组分别低 40 %、5 4% (P <0 .0 1) ;线粒体Ca2 +的摄入量较对照组分别减少 6 7%、85 % (P <0 .0 1) ,线粒体Ca2 +释放率 (11%、8% )降低与对照组 (14% )相比差异显著 (P <0 .0 5、P <0 .0 1)。NO合酶抑制剂左旋硝基精氨酸甲酯 (L NAME ,10 - 4 mol L)与相同浓度的L Arg共同孵育的线粒体 ,明显抑制了L Arg对线粒体的效应 ,与单纯L Arg组比较 ,NO2 生成减少 ,线粒体钙含量和反映线粒体45Ca2 +的摄入与释放能力都接近对照组水平。结论 :心肌线粒体L 精氨酸 一氧化氮系统参与了线粒体对心肌细胞Ca2 +浓度的调节 。

Aim and Methods: To observe the effect of myocardial mitochondrial L-arginine(L-Arg) /nitric oxide (NO) system on mitochondrial Ca 2+ transport by using purified rat mitochondria and incubation of them in vitro. Results: Compared with control group, incubation of mitochondria with L-Arg (10 -4mol/L,NO substrate) or sodium nitroprusside (5×10 -7mol/L, the donor of exogenous NO,SNP) increased significantly mitochondrial NO - 2 (66 % and 89%, P<0.01), respectively, and decreased the Ca 2+ content (40% and 54%, P<0.01). After L-Arg or SNP treatment, mitochondrial Ca 2+ uptake were decreased by 67% and 85%, respectively (P<0.01), vs control. The rate of mitochondrial Ca 2+ release decreased by 11% and 8% , respectively (P<0.01). When L-NAME (NO synthase inhibitor) was incubated with mitochondria and the L-Arg together, it inhibited the effects of L-Arg, NO 2 on the mitochondrial NO2 formation, Ca 2+ content descending, and decrease of Ca 2+ uptake and release. Conclusion: The data suggest that myocardial mitochondrial L-Arg /NO sytems take part in the regulation of cardiomyocytes Ca 2+ transportation.