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低肾素性原发性高血压和肾实质高血压中肾激肽释放酶活性受抑制的机制。

Mechanisms of suppression of renal kallikrein activity in low renin essential hypertension and renoparenchymal hypertension.

作者信息

Shimamoto K, Masuda A, Ando T, Ura N, Nakagawa M, Mori Y, Nakagawa H, Sakakibara T, Ogata H, Iimura O

机构信息

Second Department of Internal Medicine, Sapporo Medical College, Japan.

出版信息

Hypertension. 1989 Oct;14(4):375-8. doi: 10.1161/01.hyp.14.4.375.

Abstract

The mechanism of suppression of renal kallikrein activity in low renin essential hypertensive and renoparenchymal hypertensive patients was investigated in this study. From Sephadex G-200 column chromatography studies, a single kallikrein peak was observed in both kallikrein radioimmunoassay and kininogenase activity in all samples from normal subjects, low renin essential hypertensive and renoparenchymal hypertensive patients, and in purified kallikrein solution. The enzyme-specific activity around the kallikrein peak in all urine samples from each group was significantly lower than that in purified kallikrein, and a significantly lower specific activity was found in both patient groups than was found in normal subjects. Moreover, it was also recognized that the specific activity of kallikrein decreased in all cases with the increase of the molecular weight of kallikrein, and this tendency was observed more obviously in the low renin essential hypertensive and renoparenchymal hypertensive patients than in the normal subjects. These results suggest the presence of a kallikrein-specific inhibitor with a low molecular weight in human urine, although the possibility of a variant form of kallikrein cannot be excluded.

摘要

本研究调查了低肾素原发性高血压患者和肾实质高血压患者肾激肽释放酶活性受抑制的机制。通过葡聚糖凝胶G - 200柱层析研究,在正常受试者、低肾素原发性高血压患者和肾实质高血压患者的所有样本以及纯化的激肽释放酶溶液中,激肽释放酶放射免疫测定和激肽原酶活性均观察到单一的激肽释放酶峰。每组所有尿液样本中激肽释放酶峰周围的酶比活性均显著低于纯化激肽释放酶,且两个患者组的比活性均显著低于正常受试者。此外,还发现随着激肽释放酶分子量的增加,所有情况下激肽释放酶的比活性均降低,并且这种趋势在低肾素原发性高血压患者和肾实质高血压患者中比在正常受试者中更为明显。这些结果表明人尿中存在一种低分子量的激肽释放酶特异性抑制剂,尽管不能排除存在激肽释放酶变异形式的可能性。

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