1. Genetic Abrogation of Adenosine A3 Receptor Prevents Uninephrectomy and High Salt–Induced Hypertension
- Author
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Ting Yang, Christa Zollbrecht, Malin E. Winerdal, Zhengbing Zhuge, Xing‐Mei Zhang, Niccolo Terrando, Antonio Checa, Johan Sällström, Craig E. Wheelock, Ola Winqvist, Robert A. Harris, Erik Larsson, A. Erik G. Persson, Bertil B. Fredholm, and Mattias Carlström
- Subjects
adenosine receptor ,cardiovascular disease ,high salt diet ,inflammation ,kidney ,nephron number ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
BackgroundEarly‐life reduction in nephron number (uninephrectomy [UNX]) and chronic high salt (HS) intake increase the risk of hypertension and chronic kidney disease. Adenosine signaling via its different receptors has been implicated in modulating renal, cardiovascular, and metabolic functions as well as inflammatory processes; however, the specific role of the A3 receptor in cardiovascular diseases is not clear. In this study, gene‐modified mice were used to investigate the hypothesis that lack of A3 signaling prevents the development of hypertension and attenuates renal and cardiovascular injuries following UNX in combination with HS (UNX‐HS) in mice. Methods and ResultsWild‐type (A3+/+) mice subjected to UNX‐HS developed hypertension compared with controls (mean arterial pressure 106±3 versus 82±3 mm Hg; P
- Published
- 2016
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