孕期高糖饮食对子代血管紧张素Ⅱ介导的升压反应和血管张力的影响及机制

发布时间：2018-05-09 05:55

本文选题：血管紧张素II + 钙通道　；参考：《苏州大学》2014年硕士论文

【摘要】：目的：研究孕期高糖饮食对其成年子代血管紧张素II介导的升压反应和血管张力的影响及其机制。方法：怀孕的母鼠在整个孕期内被供以20%的糖水。检测其成年子代血管紧张素II介导的升压反应及其对肠系膜血管的收缩反应。在成年子代的肠系膜血管平滑肌细胞上检测L型钙通道（Cav1.2）的电流。结果：高糖组成年子代血管紧张素II介导的升压反应高于正常组。在高糖组成年子代肠系膜上，AT1受体而非AT2受体介导了血管紧张素II作用的增强；PKC阻断剂GF109203X抑制了血管紧张素II作用的增强；PKC激动剂PDBu产生了更强的收缩反应，并且这种反应的增强能够被Cav1.2阻断剂nifedipine抑制；PKCα表达增加，但PKCδ表达没有改变；KCl引起的收缩更强，并且这种收缩的增强能被nifedipine抑制；nifedipine还能减少血管紧张素II收缩作用的增强。此外，，高糖成年子代肠系膜血管平滑肌细胞上的Cav1.2表现出了更大的电流密度，但它的表达没有明显改变。结论：孕期高糖饮食改变了血管紧张素II介导的升压反应和血管张力，这种改变与PKC/Cav1.2通路的增强有关，而PKC/Cav1.2通路的增强可能是由AT1受体，PKCα和Cav1.2的改变导致的。
[Abstract]:Aim: to study the effects of high glucose diet during pregnancy on angiotensin II mediated pressor response and vascular tension in adult offspring. Methods: pregnant rats were given 20% sugar water throughout the pregnancy. The vasoconstriction of mesenteric vessels and the pressor response mediated by angiotensin II in adult offspring were measured. The current of L-type calcium channel Cav1.2 was detected in mesenteric vascular smooth muscle cells of adult offspring. Results: the pressor response mediated by angiotensin II was higher in the annual offspring with high glucose composition than that in the normal group. AT1 receptor on the mesenteric mesentery of high glucose composition, instead of AT2 receptor, mediates the enhancement of angiotensin II antagonist GF109203X, which inhibits the contractile response of angiotensin II enhanced PKC agonist PDBu. The enhancement of this reaction could be inhibited by the Cav1.2 blocker nifedipine, but the expression of PKC 未 did not change the contraction induced by PKC. Moreover, the enhancement of the contraction was inhibited by nifedipine, and the increase of angiotensin II contraction was also reduced by nifedipine. In addition, Cav1.2 on mesenteric vascular smooth muscle cells of adult offspring with high glucose showed greater current density, but its expression did not change significantly. Conclusion: high glucose diet during pregnancy changes angiotensin II mediated pressor response and vascular tension, which is related to the enhancement of PKC/Cav1.2 pathway, and the enhancement of PKC/Cav1.2 pathway may be caused by the changes of AT1 receptor PKC 伪 and Cav1.2.
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R714.256

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