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血管紧张素2型受体在血管损伤后新生内膜形成中的作用。

Role of angiotensin subtype 2 receptor in neointima formation after vascular injury.

作者信息

Janiak P, Pillon A, Prost J F, Vilaine J P

机构信息

Institut de Recherches Servier, Suresnes, France.

出版信息

Hypertension. 1992 Dec;20(6):737-45. doi: 10.1161/01.hyp.20.6.737.

DOI:10.1161/01.hyp.20.6.737
PMID:1452289
Abstract

The role of angiotensin receptor subtypes 1 and 2 was assessed on neointima formation after injury in rat carotid artery. The effects of angiotensin converting enzyme inhibition by perindopril (3 mg.kg-1 x day-1 p.o.) and selective blockade of angiotensin subtype 1 receptors by DuP 753 (5 and 30 mg.kg-1 x day-1 p.o.) were compared on proliferative response to balloon injury. In rats treated 6 days before and for 14 days after injury, perindopril significantly reduced (-76%, p < 0.01) myointimal hyperplasia. In contrast, DuP 753 at 5 mg.kg-1 x day-1 did not modify the hyperplastic response to balloon catheterization. Only at 30 mg.kg-1 x day-1 was DuP 753 able to reduce neointima formation (-47%, p < 0.05). This dose was equipotent to perindopril on the renin-angiotensin system as assessed by the pressor response to angiotensin II and angiotensin I. Therefore, blockade of subtype 1 receptors was a less effective means of suppression of myointimal growth than angiotensin converting enzyme inhibition, suggesting that another angiotensin receptor subtype or converting enzyme substrates are involved in this process. For the determination of whether angiotensin subtype 2 receptors were implicated, the specific subtype 2 receptor antagonist CGP 42112A (1 mg.kg-1 x day-1) was continuously infused perivascularly for 14 days in the vicinity of the injured carotid artery. CGP 42112A was as effective in preventing neointima formation as perindopril (-73%, p < 0.01, versus -76%, p < 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了血管紧张素受体1型和2型在大鼠颈动脉损伤后新生内膜形成中的作用。比较了培哚普利(3mg·kg-1·d-1口服)抑制血管紧张素转换酶以及杜普753(5和30mg·kg-1·d-1口服)选择性阻断血管紧张素1型受体对球囊损伤后增殖反应的影响。在损伤前6天及损伤后14天给药的大鼠中,培哚普利显著减少了肌内膜增生(-76%,p<0.01)。相比之下,5mg·kg-1·d-1的杜普753并未改变对球囊导管插入术的增生反应。仅在30mg·kg-1·d-1时,杜普753能够减少新生内膜形成(-47%,p<0.05)。通过对血管紧张素II和血管紧张素I的升压反应评估,该剂量在肾素-血管紧张素系统方面与培哚普利等效。因此,阻断1型受体抑制肌内膜生长的效果不如抑制血管紧张素转换酶,这表明该过程涉及另一种血管紧张素受体亚型或转换酶底物。为了确定血管紧张素2型受体是否参与其中,在损伤的颈动脉附近血管周围持续输注特异性2型受体拮抗剂CGP 42112A(1mg·kg-1·d-1)14天。CGP 42112A在预防新生内膜形成方面与培哚普利同样有效(分别为-73%,p<0.01和-76%,p<0.01)。(摘要截断于250字)

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