Anderson W P
Baker Medical Research Institute, Melbourne, Vic., Australia.
Blood Press Suppl. 1994;5:57-60.
This paper reviews briefly the experimental support for the hypothesis that hypertrophy of the walls of pre-glomerular vessels may occur in human essential hypertension and in spontaneously hypertensive rats (SHR) and that it may be the primary stimulus to the development of the hypertension. Pre-glomerular hypertrophy with resultant lumen narrowing will simulate narrowing of the main renal artery haemodynamically, as originally proposed by Goldblatt. In SHR there is strong evidence for increased wall thickness of the intra-renal arteries and for structurally based narrowing of the lumen of the afferent arterioles. Compatible with these morphological findings, SHR have increased resting renal vascular resistance and it has been shown experimentally that the extent of increased renal resistance is correlated with the extent of hypertension development. Increased renal vascular resistance occurs early in human essential hypertension too, but direct evidence for pre-glomerular structural changes is lacking and will be difficult to gather. The causes of the pre-glomerular structural changes in SHR remain to be determined, but they do not appear to be secondary to the hypertension.
在人类原发性高血压和自发性高血压大鼠（SHR）中，肾小球前血管壁可能会发生肥大，并且这可能是高血压发展的主要刺激因素。如Goldblatt最初提出的那样，肾小球前肥大导致管腔狭窄，在血流动力学上会模拟主肾动脉狭窄。在SHR中，有强有力的证据表明肾内动脉壁厚度增加，以及入球小动脉管腔基于结构的狭窄。与这些形态学发现相符的是，SHR的静息肾血管阻力增加，并且实验表明肾阻力增加的程度与高血压发展的程度相关。肾血管阻力增加在人类原发性高血压中也出现得较早，但缺乏肾小球前结构变化的直接证据，且难以收集。SHR中肾小球前结构变化的原因仍有待确定，但它们似乎并非继发于高血压。
