Lindsey C J, de Paula U M, Paiva A C
Hypertension. 1983 Nov-Dec;5(6 Pt 3):V134-7. doi: 10.1161/01.hyp.5.6_pt_3.v134.
Intravenous infusion of the converting-enzyme (CE) inhibitor, MK422 (1 mg X kg-1 X hr-1 for 30 minutes) in normotensive controls and two-kidney, one clip (2K1C) rats in the acute phase of renovascular hypertension had a significant hypotensive effect that persisted after 24 hours. In contrast to that prolonged effect, inhibition of the pressor responses to intraarterial or intravenous angiotensin I, and the potentiation of the depressor responses to intravenous bradykinin (BK), were evident during the hour following the infusion of MK422, but not 24 hours later. Potentiation of intraarterially administered BK, however, persisted for 24 hours after infusion of the CE inhibitor. It is concluded that at least the prolonged (24-hour) effect of the treatment with MK422 was due to inhibition of the CE activity in tissues other than the lung, and that increased levels of endogenous BK may be responsible for the inhibitor's hypotensive effect.
在血压正常的对照组以及处于肾血管性高血压急性期的双肾单夹（2K1C）大鼠中，静脉输注转化酶（CE）抑制剂MK422（1毫克/千克/小时，持续30分钟）具有显著的降压作用，且该作用在24小时后仍持续存在。与这种长效作用相反，在输注MK422后的1小时内，对动脉内或静脉内血管紧张素I的升压反应受到抑制，以及对静脉注射缓激肽（BK）的降压反应增强是明显的，但24小时后则不明显。然而，动脉内给予BK的增强作用在输注CE抑制剂后持续24小时。得出的结论是，至少MK422治疗的长效（24小时）作用是由于抑制了肺以外组织中的CE活性，并且内源性BK水平的升高可能是该抑制剂降压作用的原因。
