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慢性糖尿病大鼠的血管和肾上腺肾素样活性

Vascular and adrenal reninlike activity in chronically diabetic rats.

作者信息

Ubeda M, Hernandez I, Fenoy F, Quesada T

机构信息

Department of Physiology, Faculty of Medicine, University of Murcia, Spain.

出版信息

Hypertension. 1988 Apr;11(4):339-43. doi: 10.1161/01.hyp.11.4.339.

Abstract

The aim of this work was to investigate, in an experimental model of diabetes mellitus, the levels of renin activity in vascular and adrenal tissues and their relationship to several circulating renin-angiotensin system components. Rats with chronic (12 weeks) streptozocin-induced diabetes showed a significant decrease in plasma renin activity (PRA), plasma renin concentration, and plasma aldosterone. However, plasma trypsin activatable inactive renin concentration was increased (11.65 +/- 1.40 vs 6.73 +/- 0.57 ng angiotensin I/ml/hr; p less than 0.001), as were aortic reninlike activity (p less than 0.001) and adrenal renin, both in the zona glomerulosa (p less than 0.01) and the fascicular-reticular-medullary portion (p less than 0.001) with respect to an age-matched control group. After bilateral nephrectomy, plasma renin-angiotensin system components (PRA and plasma active and inactive renin concentrations) as well as aortic and fascicular-reticular-medullary renin activity significantly decreased in both control and diabetic rats. However, glomerular renin activity increased in control nephrectomized rats to the levels observed in diabetic animals but did not change in diabetic nephrectomized rats. The parallel changes of aortic and fascicular-reticular-medullary renin activity and plasma inactive renin concentration in diabetes and nephrectomy suggest an interdependent relationship, whereas the increase of glomerular renin activity in diabetic and nephrectomized animals, both with low levels of PRA, suggests the existence of a local autonomic renin-angiotensin system regulated by plasma feedback. Tissue renin-angiotensin system alterations in diabetes could mean that a pathogenic factor is involved in long-term diabetic complications or that only a compensatory physiological process is at work.

摘要

本研究旨在通过糖尿病实验模型,探究血管和肾上腺组织中的肾素活性水平及其与几种循环肾素 - 血管紧张素系统成分的关系。慢性(12周)链脲佐菌素诱导的糖尿病大鼠血浆肾素活性(PRA)、血浆肾素浓度和血浆醛固酮显著降低。然而,血浆胰蛋白酶可激活的无活性肾素浓度升高(11.65±1.40对6.73±0.57 ng血管紧张素I/ml/小时;p<0.001),主动脉肾素样活性(p<0.001)和肾上腺肾素也升高,相对于年龄匹配的对照组,球状带(p<0.01)和束状 - 网状 - 髓质部分(p<0.001)均如此。双侧肾切除术后,对照组和糖尿病大鼠的血浆肾素 - 血管紧张素系统成分(PRA以及血浆活性和无活性肾素浓度)以及主动脉和束状 - 网状 - 髓质肾素活性均显著降低。然而,对照肾切除大鼠的肾小球肾素活性升高至糖尿病动物观察到的水平,但糖尿病肾切除大鼠未发生变化。糖尿病和肾切除时主动脉和束状 - 网状 - 髓质肾素活性以及血浆无活性肾素浓度的平行变化提示存在相互依存关系,而糖尿病和肾切除动物(两者PRA水平均低)肾小球肾素活性的升高提示存在受血浆反馈调节的局部自主肾素 - 血管紧张素系统。糖尿病时组织肾素 - 血管紧张素系统的改变可能意味着致病因素参与长期糖尿病并发症,或者仅存在代偿性生理过程。

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