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急性缺氧和血管紧张素Ⅱ对血管内皮细胞分泌内皮素功能的影响 被引量:2

Effects of acute hypoxia and angiotensin Ⅱ on endothelin-secretory function of vascular endothelial cells
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摘要 目的观察急性缺氧和血管紧张素Ⅱ对培养的血管内皮细胞分泌内皮素的影响。方法将培养的血管内皮细胞分为空白对照组、单纯缺氧组、血管紧张素Ⅱ组和血管紧张素Ⅱ联合缺氧组(其中AgⅡ组和AgⅡ同缺氧联合组又根据AgⅡ在培养液中的终浓度分别设高、中、低浓度组)。采用低压舱对培养的血管内皮细胞进行缺氧,采用放免法测定各组样本细胞培养液中的内皮素浓度。结果①急性缺氧可引起血管内皮细胞分泌血管内皮素含量明显增高。②血管紧张素Ⅱ亦显著促进血管内皮细胞分泌血管内皮素,尤以中等浓度血管紧张素Ⅱ作用明显。③急性缺氧加血管紧张素Ⅱ对血管内皮细胞分泌血管内皮素的影响明显强于其单一因素的影响。④无论是单纯缺氧、单纯血管紧张素Ⅱ作用,还是缺氧与血管紧张素Ⅱ联合作用于血管内皮细胞于作用后0.5h分泌内皮素即增加,作用后6h达高峰,作用后24h有所降低。结论急性缺氧和血管紧张素Ⅱ均具有促进血管内皮细胞分泌内皮素的作用,且两者具有协同作用。其生理效应与其剂量和时间相关联。 Objective To observe the effect of acute hypoxia and angiotensin Ⅱ on endothelin-secretion by vascular endothelial cells. Methods Cultured vascular endothelial cells were divided into the groups of control, hypoxia, angiotensin Ⅱ , and combination of angiotensin Ⅱ plus hypoxia. Altitude chamber was used to create a hypoxic environment for vascular endothelial cells. The concentrations of endothelin in cultured liquid were measured by radioimmunoassay. Results ①Acute hypoxia induced high endothelin secretion of the vascular endothelial cells. ②Angiotensin Ⅱ also significantly promoted high endothelin secretion of vascular endothelial cells, especially more significant in the median concentration group of angiotensin Ⅱ. ③The effect of combination of hypoxia plus angiotensin Ⅱ on endothelin secretion of vascular endothelial cells was significantly stronger than that of hypoxia or of angiotensin Ⅱ alone. ④Single hypoxia,single angiotensin Ⅱ , or a combination of hypoxia plus angiotensin Ⅱ began to increase the endotholin secretion of vascular endothelial cells in 30 min after their action, the peak value of secretion being in 6 h after action; 24 h after action saw the action fade. Conclusion Both hypoxia and angiotensin Ⅱ stimulate vascular endothelial cells to secrete more endothelin,showing a synergetic action; their physiological effects correlate with dosage used and time.
出处 《山西医药杂志》 CAS 2005年第9期718-721,共4页 Shanxi Medical Journal
基金 海军后勤科研基金资助项目(003321)
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参考文献16

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