血浆肾素活性及组织血管紧张素转换酶的变化

Plasma renin activity and changes in tissue angiotensin converting enzyme.

作者信息

Michel B, Grima M, Stephan D, Coquard C, Welsch C, Barthelmebs M, Imbs J L

机构信息

Institut de Pharmacologie (URA D0589 CNRS), Université Louis Pasteur, Strasbourg, France.

出版信息

J Hypertens. 1994 May;12(5):577-84.

PMID:7930558

Abstract

OBJECTIVES

Recent evidence suggests that tissue generation of angiotensins I and II depends on the level of the plasma components of the renin-angiotensin system and on tissue-specific processes. The present study was undertaken to clarify the possible relationship between plasma renin activity (PRA) and tissue angiotensin converting enzyme (ACE) activity in the heart, lung, kidney cortex and kidney medulla of Wistar-Kyoto rats. In the kidney cortex particular attention was focused on renal brush-border ACE.

METHODS

Different experimental models known to have opposite effects on PRA were used: changes in salt intake, deoxycorticosterone acetate (DOCA) with or without salt supplements, and the Goldblatt two-kidney, one clip (2-K,1C) model. Two weeks after the start of the experiments the rats were killed, and PRA, and plasma and tissue ACE activity, were measured.

RESULTS

At the end of the study the blood pressure in the treated rats was not significantly different from control. As expected, the PRA were highest in the 2-K,1C and depleted-salt groups and lowest in the DOCA, DOCA-salt and high-salt groups. ACE responses were different in different types of tissue, with no relationship between PRA and plasma or tissue ACE activity. For example, DOCA treatment led to increased ACE activity in the heart and the kidney only if the rats were maintained on a high salt intake. DOCA or salt alone failed to have this effect. In the 2-K,1C model the unclipped kidneys did not show any significant variation in ACE activity, but the clipped kidneys exhibited increased ACE activity compared with sham-operated rats. This increase, coupled with increased renal renin secretion, could play a role in the acceleration of local angiotensin II formation, and could thus initiate and sustain the development of hypertension in this model.

CONCLUSION

The present results show that variations in ACE activity were organ-specific and were not linked either to hypertension or to changes in PRA.

摘要

目的

最近有证据表明，血管紧张素I和II的组织生成取决于肾素-血管紧张素系统的血浆成分水平以及组织特异性过程。本研究旨在阐明Wistar-Kyoto大鼠心脏、肺、肾皮质和肾髓质中血浆肾素活性（PRA）与组织血管紧张素转换酶（ACE）活性之间的可能关系。在肾皮质中，特别关注肾刷状缘ACE。

方法

使用已知对PRA有相反作用的不同实验模型：盐摄入量的变化、有或无盐补充剂的醋酸脱氧皮质酮（DOCA），以及Goldblatt双肾单夹（2-K，1C）模型。实验开始两周后处死大鼠，测量PRA、血浆和组织ACE活性。

结果

研究结束时，治疗组大鼠的血压与对照组无显著差异。正如预期的那样，PRA在2-K，1C组和低盐组中最高，在DOCA、DOCA-盐组和高盐组中最低。不同类型组织中的ACE反应不同，PRA与血浆或组织ACE活性之间没有关系。例如，只有当大鼠维持高盐摄入时，DOCA治疗才会导致心脏和肾脏中的ACE活性增加。单独使用DOCA或盐均未产生此效果。在2-K，1C模型中，未夹闭的肾脏ACE活性没有任何显著变化，但与假手术大鼠相比，夹闭的肾脏ACE活性增加。这种增加，再加上肾素分泌增加，可能在局部血管紧张素II形成的加速中起作用，从而启动和维持该模型中高血压的发展。