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达伊瓦盐敏感和盐抵抗大鼠中的尿激肽释放酶

Urinary kallikrein in Dahl-Iwai salt-sensitive and -resistant rats.

作者信息

Yoshida H, Nakagawa M, Aoyama T, Takizawa H, Higashiura K, Ura N, Shimamoto K

机构信息

Second Department of Internal Medicine, Sapporo Medical University, School of Medicine, Chuo-Ku, Japan.

出版信息

Am J Hypertens. 1997 May;10(5 Pt 2):73S-77S.

PMID:9160785
Abstract

This study was designed to evaluate the differences between the renal kallikrein in newly established Dahl-Iwai rats under salt loading and that of Sprague-Dawley rats (SD). Urinary kallikrein quantity and activity was markedly lower in Dahl-Iwai rats than in SD even during the control period. Moreover, kallikrein quantity and activity in Dahl-Iwai salt-sensitive rats (SS) were clearly diminished in comparison with salt-resistant rats (SR). The kallikrein activity/ quantity ratio was also lower in SS and SR than in SD during the control period. After salt loading, systolic blood pressure increased only in SS. Kallikrein activity in SS and SR, and kallikrein quantity in SS were increased, whereas those in SD did not change. Although the kallikrein activity/quantity ratio in SR reached the same level in SD after salt loading, that in SS was lower throughout the experiment. These results suggest that Dahl-Iwai rats are less able hereditarily to produce renal kallikrein and that there may exist structurally abnormal kallikrein that may have a lower activity. Different kinetics of renal kallikrein between SS and SR by salt loading might be explained by kallikrein inhibitors or abnormal kallikrein or nonkallikrein kininogenase. These different kinetics of renal kallikrein may play some role on blood pressure elevation in SS.

摘要

本研究旨在评估盐负荷条件下新建立的 Dahl-Iwai 大鼠与 Sprague-Dawley 大鼠(SD 大鼠)肾脏激肽释放酶之间的差异。即使在对照期,Dahl-Iwai 大鼠的尿激肽释放酶量和活性也明显低于 SD 大鼠。此外,与盐抵抗大鼠(SR)相比,Dahl-Iwai 盐敏感大鼠(SS)的激肽释放酶量和活性明显降低。在对照期,SS 和 SR 的激肽释放酶活性/量比值也低于 SD 大鼠。盐负荷后,仅 SS 的收缩压升高。SS 和 SR 的激肽释放酶活性以及 SS 的激肽释放酶量增加,而 SD 大鼠的这些指标未发生变化。尽管盐负荷后 SR 的激肽释放酶活性/量比值达到了 SD 大鼠的相同水平,但在整个实验过程中 SS 的该比值较低。这些结果表明,Dahl-Iwai 大鼠遗传性地产生肾脏激肽释放酶的能力较低,并且可能存在结构异常、活性较低的激肽释放酶。盐负荷导致 SS 和 SR 之间肾脏激肽释放酶的不同动力学变化,这可能由激肽释放酶抑制剂、异常激肽释放酶或非激肽释放酶激肽原酶来解释。这些肾脏激肽释放酶的不同动力学变化可能在 SS 的血压升高中起一定作用。

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