Kidney Renin Release under Hypoxia and Its Potential Link with Nitric Oxide: A Narrative Review
Weiwei Kong,
Yixin Liao,
Liang Zhao,
Nathan Hall,
Hua Zhou,
Ruisheng Liu,
Pontus B. Persson,
Enyin Lai
Affiliations
Weiwei Kong
Kidney Disease Center of First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
Yixin Liao
Department of Obstetrics and Gynaecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
Liang Zhao
Department of Nephrology, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou 310052, China
Nathan Hall
Department of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
Hua Zhou
Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang 110004, China
Ruisheng Liu
Department of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
Pontus B. Persson
Institute of Translational Physiology, Charité–Universitätsmedizin Berlin, 10117 Berlin, Germany
Enyin Lai
Kidney Disease Center of First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
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.
