Transient hyperosmolality modulates expression of cardiac aquaporins

• Published in: Biochemical and biophysical research communications 2012-08, Vol.425 (1), p.70-75
• Main Authors: Rutkovskiy, Arkady, Mariero, Lars Henrik, Nygård, Ståle, Stensløkken, Kåre-Olav, Valen, Guro, Vaage, Jarle
• Format: Article
• Language: English
• Subjects: Animals; Aquaporin 1 - biosynthesis; Aquaporin 4 - biosynthesis; Brain - metabolism; Cardiac aquaporins; Heart water balance; Hyperosmolality; Mice; Mice, Inbred C57BL; Myocardial edema; Myocardium - metabolism; Osmolar Concentration; Osmotherapy; Plasma - physiology; Plasma osmolality
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2012.07.052

► Backround: aquaporins (AQPs) are regulated by osmolarity in brain and kidney. ► We show that cardiac AQP1 and 4 are also regulated by osmolarity. ► Cardiac AQPs are regulated in the same time frame as in the brain. ► Regulation occurs on transcriptional, translational and post-translational levels. Hyperosmolarity is a common complication in intensive care patients, dysregulating water balance in many organs including brain and heart. The aquaporin (AQP) water channels, in particular AQP1 and −4, have been suggested to play an important role in fluid homeostasis of the myocardium. In many organs AQP expression is regulated by osmolarity, drastically altering water permeability of the cell membranes. The aim of our study was to investigate if plasma hyperosmolality may regulate cardiac expression of AQP1 and −4, and if so, at which magnitude and time frame such regulation takes place. C57Bl6 mice were injected intraperitoneally with either 1.5ml 0.154Mol (isoosmotic), 0.5ml 1Mol (mild hyperosmotic) or 0.5ml 2Mol (strong hyperosmotic) NaCl. Plasma, hearts, and forebrains were harvested before injection (“time 0”), and after 1, 4, 8 and 24h. AQP1 and −4 expression were analyzed using qPCR and Western blot. Isoosmotic and mild hyperosmotic injections caused no important changes in cardiac AQP expression. Strong hyperosmotic NaCl injections induced an upregulation of AQP1 mRNA and glycosylated fraction of AQP1 protein in the heart without changes of the total protein. AQP4 mRNA and protein decreased in the heart and increased in the brain after hyperosmotic NaCl. The change in AQP4 protein content in the brain preceded the increase of mRNA. As in the brain, expression of AQP1 and −4 in the heart is influenced by changes in plasma osmolality. Changes in AQP expression may alter cardiac function in hyperosmotic states.