Safar M E, van Bortel L M, Struijker-Boudier H A
Department of Internal Medicine, Broussais Hospital, Paris, France.
J Vasc Res. 1997 Mar-Apr;34(2):67-81. doi: 10.1159/000159204.
Alterations in the structure of resistance and conduit arteries are a characteristic hallmark in hypertension. Studies carried out in hypertensive rats and in humans suggest that angiotensin I-converting enzyme inhibition has an effect on arterial structure of resistance arteries. In hypertensive rats the reduction of the media to lumen ratio is dose-dependent and significantly different from the effects of other antihypertensive agents at doses causing an equal degree of blood pressure reduction. In large conduit arteries, hypertrophy of the vessels is reversed by converting enzyme inhibition both in hypertensive rats (studies on central arteries) and in human (studies on peripheral arteries) hypertension. The reduction of hypertrophy is associated with a decrease in arterial stiffness, partly independent of blood pressure reduction. These findings suggest that regression of structural vascular changes may contribute to both the decrease in the arteriolar resistance and the improvement in the buffering function of large arteries. The decrease in arteriolar resistance and the improvement of large artery compliance may participate in blood pressure reduction and an improvement in pulse pressure amplification produced by converting enzyme inhibition.
阻力动脉和输送动脉结构的改变是高血压的一个典型特征。在高血压大鼠和人类中进行的研究表明，血管紧张素I转换酶抑制对阻力动脉的动脉结构有影响。在高血压大鼠中，中膜与管腔比值的降低呈剂量依赖性，且与其他降压药物在同等程度降低血压剂量时的效果有显著差异。在大的输送动脉中，无论是高血压大鼠（对中心动脉的研究）还是人类（对周围动脉的研究），血管紧张素转换酶抑制都能逆转血管的肥厚。肥厚的减轻与动脉僵硬度的降低有关，部分独立于血压的降低。这些发现表明，血管结构变化的逆转可能有助于小动脉阻力的降低和大动脉缓冲功能的改善。小动脉阻力的降低和大动脉顺应性的改善可能参与了血管紧张素转换酶抑制所导致的血压降低和脉压放大的改善。
