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缓激肽对远端肾单位中由ENaC介导的钠重吸收的调控

Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin.

作者信息

Mamenko Mykola, Zaika Oleg, Boukelmoune Nabila, Madden Eric, Pochynyuk Oleh

机构信息

Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas, USA.

Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas, USA.

出版信息

Vitam Horm. 2015;98:137-54. doi: 10.1016/bs.vh.2014.12.005. Epub 2015 Feb 14.

DOI:10.1016/bs.vh.2014.12.005
PMID:25817868
Abstract

Kinins, such as Bradykinin (BK), are peptide hormones of the kallikrein-kinin system. Apart from being a vasodilator, BK also increases urinary sodium excretion to reduce systemic blood pressure. It is becoming appreciated that BK modulates function of the epithelial Na(+) channel in the distal part of the renal nephron to affect tubular sodium reabsorption. In this chapter, we outline the molecular details, as well as discuss the physiological relevance of this regulation for the whole organism sodium homeostasis and setting chronic blood pressure.

摘要

激肽,如缓激肽(BK),是激肽释放酶-激肽系统的肽类激素。除了作为一种血管舒张剂外,BK还能增加尿钠排泄以降低全身血压。人们逐渐认识到,BK可调节肾单位远端上皮钠通道的功能,从而影响肾小管对钠的重吸收。在本章中,我们概述了分子细节,并讨论了这种调节对整个机体钠稳态和慢性血压调节的生理意义。

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Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin.缓激肽对远端肾单位中由ENaC介导的钠重吸收的调控
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引用本文的文献

1
Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac Hypertrophy.肾脏中缓激肽的慢性过表达会导致多尿和心脏肥大。
Front Med (Lausanne). 2018 Dec 3;5:338. doi: 10.3389/fmed.2018.00338. eCollection 2018.