Pörsti I, Säynävälammi P, Arvola P, Nurmi A K, Manninen V, Ylitalo P, Vapaatalo H
Methods Find Exp Clin Pharmacol. 1986 Sep;8(9):543-6.
Possible non-renin antihypertensive actions of two angiotensin-converting enzyme inhibitors, the sulfhydryl compound captopril and the new nonsulfhydryl inhibitor quinapril (CI-906), were compared in rats with one-kidney deoxycorticosterone-salt hypertension. Plasma renin activity remained low during the 12-day treatments and showed very strong suppression of the renin-angiotensin system. Quinapril did not influence the rapidly increasing blood pressure. Although captopril tended to reduce the development of hypertension (p = 0.08), it did not have any significant effect, either. The results indicate that these ACE inhibitors with different chemical structures lack any significant blood pressure lowering mechanism in severe deoxycorticosterone-salt hypertension, a model in which they cannot act through their established antihypertensive mechanism, the inhibition of the renin-angiotensin system.
在一侧肾脱氧皮质酮-盐性高血压大鼠中，比较了两种血管紧张素转换酶抑制剂（巯基化合物卡托普利和新型非巯基抑制剂喹那普利（CI-906））可能的非肾素性降压作用。在12天的治疗期间，血浆肾素活性持续处于低水平，显示肾素-血管紧张素系统受到很强的抑制。喹那普利对迅速升高的血压没有影响。虽然卡托普利有降低高血压发展趋势（p = 0.08），但也没有任何显著效果。结果表明，在严重的脱氧皮质酮-盐性高血压中，这些具有不同化学结构的血管紧张素转换酶抑制剂缺乏任何显著的降压机制，在该模型中它们无法通过其既定的降压机制（抑制肾素-血管紧张素系统）发挥作用。
