Stephan D
Service d'hypertension et des maladies vasculaires, CHRU, hôpital civil, 1, place de l'Hôpital, BP 426, 67091 Strasbourg cedex, France.
J Mal Vasc. 2007 Jul;32(3):131-4. doi: 10.1016/j.jmv.2007.04.004.
Capillary and arterioles rarefaction has been reported in animal models of hypertension and in essential and borderline hypertension. Moreover, young adults with a predisposition to hypertension may exhibit microvascular rarefaction suggesting that defective angiogenesis-arteriogenesis may be an etiological component of high blood pressure. Nevertheless, in other studies, VEGF plasma levels are increased in hypertensive subjects and low birth weight predicts higher blood pressure but not dermal capillary density. In fibrin gel chambers implanted in rats, angiogenesis-arteriogenesis are increased in spontaneously hypertensive rats (SHR) compared to their controls. In parallel, fibroblast growth factor synthesis is significantly increased in SHR fibrin gel chambers. Thus, excess in angio/arteriogenic factors synthesis could stimulate neovascularisation including resistive arterioles formation, which in turn increase peripheral vascular resistance and consequently trigger the hypertensive mechanism itself.
在高血压动物模型以及原发性高血压和临界高血压患者中,均有毛细血管和小动脉稀疏的报道。此外,易患高血压的年轻成年人可能会出现微血管稀疏,这表明血管生成-动脉生成缺陷可能是高血压的一个病因学因素。然而,在其他研究中,高血压患者的血管内皮生长因子(VEGF)血浆水平升高,低出生体重预示着更高的血压,但与皮肤毛细血管密度无关。在植入大鼠的纤维蛋白凝胶腔内,自发性高血压大鼠(SHR)的血管生成-动脉生成比其对照组增加。同时,SHR纤维蛋白凝胶腔内的成纤维细胞生长因子合成显著增加。因此,血管生成/动脉生成因子合成过多可能会刺激新血管形成,包括阻力小动脉形成,进而增加外周血管阻力,从而触发高血压机制本身。