Anderson W P, Kett M M, Evans R G, Alcorn D
Baker Medical Research Institute, Melbourne, Australia.
Blood Press Suppl. 1995;2:74-80.
This paper reviews the evidence for the occurrence of hypertrophy of the renal arterial vessels in experimental and human hypertension. In spontaneously hypertensive rats (SHR), the walls of the interlobar, arcuate and interlobular arteries appear to be hypertrophied in both the "pre-hypertensive phase" and in established hypertension. The lumen diameter of the afferent arteriole in SHR is reduced, but this is probably not due to wall hypertrophy. The renal arterial hypertrophy is not reversed by chronic angiotensin converting enzyme inhibition in SHR, in contrast to findings in other vascular beds. Renal arterial hypertrophy also occurs in other forms of hypertension including in the kidney contralateral to a renal artery stenosis, and in hypertension following sino-aortic denervation. Whilst it is not possible to document changes in wall dimensions of intrarenal arteries during the development of human hypertension, renal haemodynamic abnormalities currently attributed to renal vasoconstriction in early human hypertension are also compatible with renal arterial hypertrophy. These abnormalities include increased resting renal vascular resistance and augmented renal vascular resistance responses to vasoconstrictor agents. It is argued that hypertrophy of renal vasculature to increase pre-glomerular resistance will have dual effects: it will increase total peripheral resistance (the kidneys account for about 20% of total peripheral resistance), and it will effect renal haemodynamics distally in a manner similar to narrowing of the main renal artery. It remains to be shown experimentally whether renal arterial hypertrophy could be the primary cause of some forms of hypertension.
本文综述了实验性高血压和人类高血压中肾动脉血管肥大发生的证据。在自发性高血压大鼠（SHR）中，叶间动脉、弓形动脉和小叶间动脉的管壁在“高血压前期”和已确诊的高血压阶段似乎都有肥大。SHR传入小动脉的管腔直径减小，但这可能不是由于管壁肥大所致。与其他血管床的研究结果相反，SHR中慢性血管紧张素转换酶抑制并不能逆转肾动脉肥大。肾动脉肥大也发生在其他形式的高血压中，包括肾动脉狭窄对侧肾脏，以及去窦弓神经后高血压。虽然在人类高血压发展过程中无法记录肾内动脉壁尺寸的变化，但目前归因于早期人类高血压中肾血管收缩的肾血流动力学异常也与肾动脉肥大相符。这些异常包括静息肾血管阻力增加以及肾血管对血管收缩剂的阻力反应增强。有人认为，肾血管肥大以增加肾小球前阻力将产生双重影响：它将增加总外周阻力（肾脏约占总外周阻力的20%），并且它将以类似于主肾动脉狭窄的方式影响远端肾血流动力学。肾动脉肥大是否可能是某些形式高血压的主要原因，仍有待通过实验证明。
