Topouchian J, Brisac A M, Pannier B, Vicaut E, Safar M, Asmar R
Department of Internal Medicine and INSEM (U337) (U141), Broussais Hospital, Paris, France.
J Hum Hypertens. 1998 Mar;12(3):181-7. doi: 10.1038/sj.jhh.1000581.
In subjects with essential hypertension, angiotensin-converting enzyme (ACE) inhibition increases arterial diameter, compliance and distensibility of peripheral muscular arteries in association with blood pressure reduction. Whether pulse pressure amplification is modified by ACE inhibition and whether changes in compliance and distensibility are due to a drug effect on the arterial wall, to the blood pressure reduction or to a combination of both factors, is largely ignored. In a randomised, double-blind crossover trial, we used the ACE inhibitor quinapril as a marker to evaluate the changes in: pulse pressure amplification (applanation tonometry), carotid compliance and distensibility (echo-tracking technique), and aortic distensibility (measured from pulse wave velocity). Quinapril decreased in the same extent carotid and brachial pulse pressure, thus causing a resetting of pulse pressure amplification toward normal values. Carotid compliance and distensibility as well as aortic distensibility increased significantly. Based on three-way analysis of variance, it was shown that, whereas the changes in carotid stiffness were exclusively due to blood pressure reduction and not to a drug-induced relaxation of the arterial wall, the changes in aortic distensibility were due to the combination of both factors. Thus, using an atraumatic non-invasive procedure, it was possible to show that: (i) ACE inhibition is able to maintain pulse pressure amplification, an important factor contributing to reduce the afterload of the heart; and (ii) ACE inhibition alters the hypertensive arterial wall in a very heterogeneous manner, with a maximal drug effect on muscular large arteries like the abdominal aorta, and not on elastic arteries like the carotid artery and the thoracic aorta.
在原发性高血压患者中，血管紧张素转换酶（ACE）抑制作用在降低血压的同时，可增加外周肌性动脉的管径、顺应性和扩张性。ACE抑制作用是否会改变脉压放大，以及顺应性和扩张性的变化是由于药物对动脉壁的作用、血压降低还是两者共同作用，在很大程度上被忽视了。在一项随机、双盲交叉试验中，我们使用ACE抑制剂喹那普利作为标记物，来评估以下各项的变化：脉压放大（压平式眼压测量法）、颈动脉顺应性和扩张性（回声跟踪技术）以及主动脉扩张性（根据脉搏波速度测量）。喹那普利使颈动脉和肱动脉脉压降低程度相同，从而使脉压放大重新调整至正常值。颈动脉顺应性和扩张性以及主动脉扩张性均显著增加。基于三因素方差分析表明，虽然颈动脉僵硬度的变化完全是由于血压降低，而非药物诱导的动脉壁舒张，但主动脉扩张性的变化是由于这两个因素共同作用。因此，通过一种无创性的非侵入性方法，可以表明：（i）ACE抑制作用能够维持脉压放大，这是有助于降低心脏后负荷的一个重要因素；（ii）ACE抑制作用以一种非常不均一的方式改变高血压患者的动脉壁，对腹主动脉等肌性大动脉的药物作用最大，而对颈动脉和胸主动脉等弹性动脉的作用则不明显。
