本文選題：血管緊張素II + 鈣通道��； 參考：《蘇州大學(xué)》2014年碩士論文

【摘要】：目的：研究孕期高糖飲食對(duì)其成年子代血管緊張素II介導(dǎo)的升壓反應(yīng)和血管張力的影響及其機(jī)制。 方法：懷孕的母鼠在整個(gè)孕期內(nèi)被供以20%的糖水。檢測(cè)其成年子代血管緊張素II介導(dǎo)的升壓反應(yīng)及其對(duì)腸系膜血管的收縮反應(yīng)。在成年子代的腸系膜血管平滑肌細(xì)胞上檢測(cè)L型鈣通道（Cav1.2）的電流。 結(jié)果：高糖組成年子代血管緊張素II介導(dǎo)的升壓反應(yīng)高于正常組。在高糖組成年子代腸系膜上，AT1受體而非AT2受體介導(dǎo)了血管緊張素II作用的增強(qiáng)；PKC阻斷劑GF109203X抑制了血管緊張素II作用的增強(qiáng)；PKC激動(dòng)劑PDBu產(chǎn)生了更強(qiáng)的收縮反應(yīng)，并且這種反應(yīng)的增強(qiáng)能夠被Cav1.2阻斷劑nifedipine抑制；PKCα表達(dá)增加，但PKCδ表達(dá)沒(méi)有改變；KCl引起的收縮更強(qiáng)，并且這種收縮的增強(qiáng)能被nifedipine抑制；nifedipine還能減少血管緊張素II收縮作用的增強(qiáng)。此外，，高糖成年子代腸系膜血管平滑肌細(xì)胞上的Cav1.2表現(xiàn)出了更大的電流密度，但它的表達(dá)沒(méi)有明顯改變。 結(jié)論：孕期高糖飲食改變了血管緊張素II介導(dǎo)的升壓反應(yīng)和血管張力，這種改變與PKC/Cav1.2通路的增強(qiáng)有關(guān)，而PKC/Cav1.2通路的增強(qiáng)可能是由AT1受體，PKCα和Cav1.2的改變導(dǎo)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 偽 and Cav1.2.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R714.256

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