Vascular endothelial growth factor: A novel potential therapeutic target for hypertension

摘要

To the Editor: Hypertension is the most commonly reported side effect of angiogenesis inhibitors interfering with vascular endothelial growth factor (VEGF) signaling. A recent article by Caro and coworkers demonstrated that the increase in the use of VEGF inhibitors conditions the necessity to pay special attention to the occurrence of hypertension, and VEGF plays a key role in hypertension. This analysis suggests that VEGF may serve as a novel potential therapeutic target for hypertension. Other studies have been carried with this aim. Gennari-Moser and associates demonstrated that supernatant of endothelial cells grown in the presence of VEGF enhanced aldosterone synthase activity in human adrenocortical cells. In addition, endothelial cell-dependent and -independent activation of aldosterone is regulated by VEGF. Furthermore, Lankhorst and coworkers3 indicated that activation of the ET-1 axis may support the use of ET receptor antagonists for the treatment of angiogenesis inhibition-induced hypertension, especially because ET receptor stimulation in vascular smooth muscle cells results in VEGF production and mitogenesis in a mitogen-activated protein kinase pathway-dependent manner. What's more, Banek and colleagues showed that AMP-activated protein kinase (AMPK) is stimulated during exercise and has been shown to increase expression of VEGF. Therefore, using a potent AMPK stimulator would increase circulating VEGF, improve angiogenic potential, decrease oxidative stress, and abrogate placental ischemia-induced hypertension. In addition, Thijs and coworkers suggested a physiological role for VEGF in maintaining normal endothelial control of vasomotor tone. These findings suggest that VEGF may be a good potential therapeutic target for hypertension.