人们开始认识到抗高血压治疗的目的不仅是为了降低血压,而且也是为了预防甚至逆转血管及与高血压有关器官的损伤。测定实验动物高血压引起血管损伤的程度较容易,但测定人的血管损伤程度相当困难,然而血压与动脉直径或顺应性之间的关系可作为人动脉硬化和结构改变的一种参数。Doyle 指出甲基多巴尤其是 ACE 抑制剂,通常能逆转或预防实验及临床性高血压引起的心脏扩大、血管增生和肾损伤,但是肼酞嗪、哌唑嗪和β-肾上腺素能受体拮抗剂通常无此作用。Simon 报道高血压病人用ketanserin 或乌拉地尔治疗后,未观察到动脉顺应性的改变,而钙拮抗剂尼群地平和尼卡地平却能有效地增加动脉顺应性并加大动脉直径。Van Gilst 报道 ACE 抑制剂增加大 People began to realize that the purpose of antihypertensive treatment is not only to lower blood pressure, but also to prevent or even reverse the damage of blood vessels and organs associated with hypertension. It is relatively easy to measure the extent of vascular damage caused by hypertension in laboratory animals, but it is rather difficult to measure the degree of vascular damage in humans. However, the relationship between blood pressure and arterial diameter or compliance can be used as a parameter for arteriosclerosis and structural changes. Doyle noted that methyldopa, particularly ACE inhibitors, usually reverses or prevents heart enlargement, vascular hyperplasia and kidney damage induced by experimental and clinical hypertension, but hydralazine, prazosin, and beta-adrenergic receptors Antagonists do not usually have this effect. Simon reported no changes in arterial compliance after treatment with ketanserin or urapidil in hypertensive patients, whereas nicotine and nicardipine, a calcium antagonist, effectively increased arterial compliance and increased arterial diameter. Van Gilst reported an increase in ACE inhibitors