Bing R F, Russell G I, Swales J D, Thurston H
J Lab Clin Med. 1981 Aug;98(2):302-10.
Saralasin (Sar1, Ala8 angiotensin II), a competitive antagonist of angiotensin II, or captopril, an angiotensin-converting enzyme inhibitor, were infused for 12 hr into conscious rats with Goldblatt two-kidney one-clip hypertension at an early stage (mean interval from clipping 36 days) and a chronic stage (151 days). In the early phase infusions of either saralasin or captopril produced a significant fall in blood pressure, which was maximal at 30 min, although the majority of animals remained hypertensive. In the chronic phase, saralasin produced a small and nonsignificant fall in blood pressure, whereas captopril produced a fall similar to that observed in the early group. No further fall in blood pressure was seen over the 12 hr period. PRC was markedly elevated in the early phase but did not differ significantly from normal in the chronic phase. The blood pressure fall produced by saralasin was significantly correlated with preinfusion PRC (r = 0.72 for the early group and 0.81 for the chronic group; p less than 0.01), whereas the fall in blood pressure produced by captopril was poorly correlated with PRC (r = 0.04 and 0.14, respectively). Captopril produced a minor fall and saralasin a minor elevation of blood 3 pressure in normal animals. Infusions of dextrose without inhibitor caused no change in blood pressure. Removal of the renal artery clip normalized blood pressure in the majority (88%) of animals in either the early or chronic phases. It is concluded that 12 hr infusions of these inhibitors are no more effective than 30 min infusions and do not fully correct hypertension in this model. Furthermore, the greater vasodepressor effect of captopril compared to saralasin in chronic hypertensive animals and the lack of correlation between PRC and change in blood pressure with captopril suggest that this agent has an action independent from blockade of the renin-angiotensin system. Removal of the renal artery clip is more effective than renin-angiotensin blockade in correcting Goldblatt two-kidney one-clip hypertension.
将沙拉新（Sar1，Ala8血管紧张素II），一种血管紧张素II的竞争性拮抗剂，或卡托普利，一种血管紧张素转换酶抑制剂，对处于早期（夹闭后平均间隔36天）和慢性期（151天）的Goldblatt二肾一夹高血压清醒大鼠进行12小时输注。在早期阶段，输注沙拉新或卡托普利均使血压显著下降，30分钟时降至最大，尽管大多数动物仍处于高血压状态。在慢性期，沙拉新使血压有小幅且不显著的下降，而卡托普利产生的血压下降与早期组相似。在12小时期间未观察到血压进一步下降。早期阶段PRC显著升高，但在慢性期与正常无显著差异。沙拉新引起的血压下降与输注前PRC显著相关（早期组r = 0.72，慢性组r = 0.81；p < 0.01），而卡托普利引起的血压下降与PRC相关性较差（分别为r = 0.04和0.14）。卡托普利使正常动物血压有小幅下降，沙拉新使其有小幅升高。输注不含抑制剂的葡萄糖对血压无影响。去除肾动脉夹使大多数（88%）处于早期或慢性期的动物血压恢复正常。结论是，这些抑制剂12小时输注并不比30分钟输注更有效，且在此模型中不能完全纠正高血压。此外，在慢性高血压动物中，卡托普利比沙拉新有更大的血管减压作用，且卡托普利引起的PRC与血压变化缺乏相关性，提示该药物有独立于肾素 - 血管紧张素系统阻断的作用。去除肾动脉夹在纠正Goldblatt二肾一夹高血压方面比肾素 - 血管紧张素阻断更有效。
