Kidney Renin Release under Hypoxia and Its Potential Link with Nitric Oxide: A Narrative Review

Author:

Kong Weiwei12,Liao Yixin3,Zhao Liang4,Hall Nathan5,Zhou Hua6,Liu Ruisheng5,Persson Pontus B.7,Lai Enyin127ORCID

Affiliation:

1. Kidney Disease Center of First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China

2. Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou 310003, China

3. Department of Obstetrics and Gynaecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China

4. Department of Nephrology, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou 310052, China

5. Department of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA

6. Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang 110004, China

7. Institute of Translational Physiology, Charité–Universitätsmedizin Berlin, 10117 Berlin, Germany

Abstract

The renin–angiotensin system (RAS) and hypoxia have a complex interaction: RAS is activated under hypoxia and activated RAS aggravates hypoxia in reverse. Renin is an aspartyl protease that catalyzes the first step of RAS and tightly regulates RAS activation. Here, we outline kidney renin expression and release under hypoxia and discuss the putative mechanisms involved. It is important that renin generally increases in response to acute hypoxemic hypoxia and intermittent hypoxemic hypoxia, but not under chronic hypoxemic hypoxia. The increase in renin activity can also be observed in anemic hypoxia and carbon monoxide-induced histotoxic hypoxia. The increased renin is contributed to by juxtaglomerular cells and the recruitment of renin lineage cells. Potential mechanisms regulating hypoxic renin expression involve hypoxia-inducible factor signaling, natriuretic peptides, nitric oxide, and Notch signaling-induced renin transcription.

Funder

Natural Foundation of Zhejiang

National Natural Foundation of China

Deutsche Forschungsgemeinschaft

Joint Funds of the Zhejiang Provincial Natural Science Foundation of China

Publisher

MDPI AG

Subject

General Biochemistry, Genetics and Molecular Biology,Medicine (miscellaneous)

Reference92 articles.

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