Lever A F, Lyall F, Morton J J, Folkow B
MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland, United Kingdom.
Kidney Int Suppl. 1992 Jun;37:S51-5.
Angiotensin II (Ang II) in low dose raises blood pressure slowly by a mechanism which is not understood, but which is clearly different from the better known direct vasoconstrictor effect. Vascular hypertrophy develops during this slow pressor response, but is not wholly a consequence of the increase of pressure. We discuss non-pressor mechanisms by which Ang II may act as a growth factor to promote structural vascular change. Studies with cultured vascular smooth muscle cells suggest at least three possibilities, but none of these has been tested in vivo during slow pressor infusion of Ang II. The action of growth factors may be important in hypertension since increased arterial pressure causes vascular hypertrophy. Growth factors influence markedly the extent of this hypertrophic response and, however produced, vascular hypertrophy has an important influence on resistance and arterial pressure in hypertension.
低剂量的血管紧张素II（Ang II）通过一种尚不明确的机制缓慢升高血压，该机制显然不同于更为人熟知的直接血管收缩作用。在这种缓慢的升压反应过程中会出现血管肥大，但并不完全是压力升高的结果。我们讨论了Ang II作为生长因子促进血管结构改变的非升压机制。对培养的血管平滑肌细胞的研究提示了至少三种可能性，但在Ang II缓慢升压输注过程中，这些可能性均未在体内得到验证。生长因子的作用在高血压中可能很重要，因为动脉压升高会导致血管肥大。生长因子显著影响这种肥大反应的程度，无论血管肥大是如何产生的，它对高血压中的阻力和动脉压都有重要影响。
