Effect of NO, vasodilator prostaglandins, and adenosine on skeletal muscle angiogenic growth factor gene expression.
Effect of NO, vasodilator prostaglandins, and adenosine on skeletal muscle angiogenic growth factor gene expression.
复制标题
NO、血管扩张剂前列腺素和腺苷对骨骼肌血管生成生长因子基因表达的影响。
DOI：
10.1152/jappl.1999.86.5.1513
复制
发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Wagner,PD
中科院分区：
文献类型：
--
作者：
Benoit,H;Jordan,M;Wagner,H;Wagner,PD
运动训练导致几种肌肉适应，其中之一是血管生成。剧烈运动导致骨骼肌释放一氧化氮、前列环素（PGI2）和腺苷(A)。在本文中，我们询问这些局部释放的血管扩张剂以及其他已知的扩张性前列腺素（pge1和PGE2）是否有可能增加静息骨骼肌中血管生成生长因子的基因表达。将7组5 ~ 7只雌性Wistar大鼠（8 ~ 12周龄，体重250±10 g）麻醉后，用仪器测量颈动脉压力和电磁股动脉血流。其中一组作为对照组，其余组分别给予A（200）、硝普苷（NP, 4.2）、乙酰胆碱（100）、PGE1（1.9）、PGE2（1.7）、PGI2（1.7）等6种药物的动脉持续输注（剂量单位：μg/min）。每种药物降低周围血管阻力的程度相似（至少两倍）。NP和乙酰胆碱使血管内皮生长因子（VEGF） mRNA/18S水平升高50%，pge1和PGE2对其无影响，PGI2使其降低40%。对于碱性成纤维细胞生长因子，只有pgi2有影响，降低mRNA/18S ~ 25%。对于转化生长因子-β1， A、NP和pge1导致mRNA/18S降低，而pge2略微增加mRNA/18S。对于主要的血管生成生长因子VEGF，这些数据表明，收缩骨骼肌中自然分泌的血管扩张剂可能参与基因表达的调控，即一氧化氮的正向调控和pgi2的负向调控。
Exercise training results in several muscle adaptations, one of which is angiogenesis. Acutely, exercise leads to release of nitric oxide, prostacyclin (PGI2), and adenosine (A) in the skeletal muscles. In this paper, we asked whether any of these locally released vasodilators, as well as other known dilator prostaglandins (PGE1and PGE2), have the potential to increase angiogenic growth factor gene expression in resting skeletal muscle. Seven groups of 5–7 female Wistar rats (age 8–12 wk, weight 250 ± 10 g) were anesthetized and instrumented for carotid artery pressure and electromagnetic femoral artery blood flow measurement. One group acted as control while the other groups each received one of the following six agents by constant arterial infusion (dose in μg/min): A (200), nitroprusside (NP, 4.2), acetylcholine (100), PGE1(1.9), PGE2(1.7), and PGI2(1.7). Each agent reduced peripheral vascular resistance to a similar extent (at least twofold). Densitometric mRNA/18S levels for vascular endothelial growth factor (VEGF) were increased 50% by NP and acetylcholine, were unaffected by PGE1and PGE2, and were reduced 40% by PGI2. For basic fibroblast growth factor, only PGI2had any effect, reducing mRNA/18S ∼25%. For transforming growth factor-β1, A, NP, and PGE1led to reduced mRNA/18S, whereas PGE2slightly increased mRNA/18S. For the principal putative angiogenic growth factor, VEGF, these data suggest that naturally secreted vasodilators in contracting skeletal muscle could be involved in regulation of gene expression, namely, nitric oxide in a positive and PGI2in a negative direction.