在生理剪切应力下，暴露于不同管腔内压力水平的完整人体导管血管中内皮素-1（ET-1）和内皮型一氧化氮合酶（eNOS）表达的时间调控。
Temporal regulation of endothelial ET-1 and eNOS expression in intact human conduit vessels exposed to different intraluminal pressure levels at physiological shear stress.
作者信息
Gan L M, Selin-Sjögren L, Doroudi R, Jern S
机构信息
Clinical Experimental Research Laboratory, Heart and Lung Institute, Sahlgrenska University Hospital/Ostra, Göteborg University, SE 416 85, Gothenburg, Sweden.
出版信息
Cardiovasc Res. 2000 Oct;48(1):168-77. doi: 10.1016/s0008-6363(00)00174-7.
OBJECTIVE
By using a computerized vascular perfusion model, we investigated temporal effects of sub-acute pressure elevation on vasomotor behavior and expression of endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) in intact human conduit vessels.
METHODS
Paired umbilical veins were perfused during 1.5, 3 and 6 h under high/low intraluminal pressure (40/20 mmHg) and at identical shear stress level of 10 dyn/cm(2). ET-1 and eNOS gene and protein expression was quantified with real-time reverse-transcribed polymerase chain reaction and quantitative immunohistochemistry, respectively.
RESULTS
Pressure induced differential temporal regulation patterns of ET-1 and eNOS gene expression. During the high pressure condition, eNOS mRNA was upregulated after 3 h and leveled off after 6 h of perfusion, while ET-1 mRNA was elevated after 6 h perfusion. Immunohistochemistry verified synchronal changes at the protein level. Significant vasodilation was observed after 3 h in the high-pressure system.
CONCLUSION
Thus, subacute pressure elevation exerts differential effects on the endothelial eNOS/ET-1 expression, which dynamically regulate the vasomotor tone.
目的
通过使用计算机化血管灌注模型，我们研究了亚急性压力升高对完整人体大静脉血管舒缩行为以及内皮素-1（ET-1）和内皮型一氧化氮合酶（eNOS）表达的时间效应。
方法
配对的脐静脉在管腔内高/低压力（40/20 mmHg）下以及相同剪切应力水平10 dyn/cm²下分别灌注1.5、3和6小时。分别通过实时逆转录聚合酶链反应和定量免疫组织化学对ET-1和eNOS基因及蛋白表达进行定量分析。
结果
压力诱导了ET-1和eNOS基因表达的不同时间调节模式。在高压条件下，灌注3小时后eNOS mRNA上调，灌注6小时后趋于平稳，而ET-1 mRNA在灌注6小时后升高。免疫组织化学证实了蛋白水平的同步变化。在高压系统中，3小时后观察到显著的血管舒张。
结论
因此，亚急性压力升高对内皮eNOS/ET-1表达产生不同影响，从而动态调节血管舒缩张力。
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