Insulin resistance in spontaneously hypertensive rats is associated with endothelial dysfunction characterized by imbalance between NO and ET-1 production
Insulin resistance in spontaneously hypertensive rats is associated with endothelial dysfunction characterized by imbalance between NO and ET-1 production
复制标题
DOI：
10.1152/ajpheart.00092.2005
复制
发表时间：
2005-08-01
影响因子：
4.8
通讯作者：
Montagnani, M
中科院分区：
文献类型：
--
作者：
Potenza, MA;Marasciulo, FL;Montagnani, M
胰岛素通过激活磷脂酰肌醇 (PI)3 激酶、Akt 和内皮 NO 合酶来刺激血管内皮细胞中 NO 的产生。我们假设胰岛素抵抗可能导致内皮血管舒张剂和血管收缩剂（例如NO和ET-1）之间的不平衡，从而导致高血压。与对照 Wistar-Kyoto (WKY) 大鼠相比，12 周龄雄性自发性高血压大鼠 (SHR) 患有高血压和胰岛素抵抗（收缩压 202 +/- 11 vs. 132 +/- 10 mmHg；空腹血浆胰岛素 5 +/- 1 vs. 0.9 +/- 0.1 ng/ml；P
Insulin stimulates production of NO in vascular endothelium via activation of phosphatidylinositol (PI)3-kinase, Akt, and endothelial NO synthase. We hypothesized that insulin resistance may cause imbalance between endothelial vasodilators and vasoconstrictors (e.g., NO and ET-1), leading to hypertension. Twelve-week-old male spontaneously hypertensive rats (SHR) were hypertensive and insulin resistant compared with control Wistar-Kyoto (WKY) rats (systolic blood pressure 202 +/- 11 vs. 132 +/- 10 mmHg; fasting plasma insulin 5 +/- 1 vs. 0.9 +/- 0.1 ng/ml; P