高盐饮食对大鼠离体胸主动脉环收缩功能的影响及其机制

Effect of high-salt diet on the contraction of the rat's thoracic aorta and its mechanism

目的:观察高盐饮食早期大鼠离体胸主动脉环的收缩改变,并探讨其可能的机制。方法:雌性SD大鼠20只,随机均分成正常饮食(NC)组和高盐饮食(HS)组。喂养2w后,水合氯醛麻醉,测量动脉血压。采用大鼠离体胸主动脉环灌流,在去除血管环内皮后,观察苯肾上腺素(PE)对血管的收缩情况。先用无钙液预处理去内皮血管环,用苯肾上腺素(PE)收缩血管环,观察两组的收缩情况;再用无钙液加肝素阻断三磷酸肌醇(IP3)诱导的细胞内钙离子的释放,观察PE对两组血管环的收缩情况进而分析甘油二酯-蛋白激酶C(DG-PKC)通路的情况。结果:两组血压差异没有显著性;用无钙液预处理后再加PE,发现HS组去内皮血管环的收缩幅度显著比NC组高(P<0.01);用无钙液加肝素预处理后再加PE,发现HS组去内皮血管环的收缩幅度也显著高于NC组(P<0.01)。结论:高盐饮食大鼠早期血压虽然是正常的,但血管平滑肌对激动剂的收缩反应已经加强,这种反应可能与其细胞内钙离子浓度升高有关,其中主要是DG-PKC途径的活性增强。

Objective： To investigate the effect of high-salt diet on the contraction of the rat＇s thoracic aorta and its mechanism. Methods： Twenty female SD rats were randomly divided into normal control （NC） group and high-salt （HS） group （n=10）. After 2 weeks, the rats were anesthetized with chloral hydrate and their blood pressures were measured. Using the isolated rat＇s thoracic aorta ring perfusion model, the effect of phenylephrine （PE） on the thoracic aorta ring free of endothelia was observed. Firstly, the thoracic aorta ring without endothelia was pretreated with calcium-free liquid, then, it was contracted with PE. In this procedure, two groups＇ differences were observed. Thirdly, the release of intracellular calcium induced by 1,4,5-triphosphate inositol （IP3） was blocked using calcium-free liquid plus heparin and the path of diacylglycerol-protein kinase C （DG-PKC） was observed. Results： There were no significant difference in blood pressure in two groups. However, after the ring was pretreated with calcium-free liquid and then treated with PE, it was found that the contraction intension of the thoracic aorta ring in HS group was significantly higher than that in NC group （P〈0.01）. Conclusion： Although the blood pressure in rats fed with high-salt diet is normal in the early stage, the vascular smooth muscle contraction excited by agonist has strengthened, which may be related to the increasing intracellular calcium, especially the increasing activity of the DG-PKC pathway.