NDLI: Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats

Content Provider	Springer Nature Link
Author	Della Penna, Silvana L. Cao, Gabriel Kouyoumdzian, Nicolás M. Sarati, Lorena Fellet, Andrea Balaszczuk, Ana M. Choi, Marcelo R. Zotta, Elsa Gorzalczany, Susana Pandolfo, Marcela Toblli, Jorge E. Rosón, María I. Fernández, Belisario E.
Copyright Year	2014
Abstract	The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Groups of anesthetized male Sprague–Dawley rats were infused with isotonic saline solution (control) or with hypertonic saline solution (Na group, 1 M NaCl), either alone or with losartan (10 mg kg$^{−1}$) or tempol (0.5 mg min$^{−1}$ kg$^{−1}$) during 2 h. Renal function parameters were measured. Groups of unanesthetized animals were injected intraperitoneally with hypertonic saline solution, with or without free access to water intake, Na+W, and Na−W, respectively. The expression of AQP-1, AQP-2, Ang II, eNOS, and NF-kB were evaluated in the kidney by Western blot and immunohistochemistry. AQP-2 distribution was assessed by immunofluorescence. Na group showed increased natriuresis and diuresis, and Ang II and NF-kB expression, but decreased eNOS expression. Losartan or tempol enhanced further the diuresis, and AQP-2 and eNOS expression, as well as decreased Ang II and NF-kB expression. Confocal immunofluorescence imaging revealed labeling of AQP-2 in the apical plasma membrane with less labeling in the intracellular vesicles than the apical membrane in kidney medullary collecting duct principal cells both in C and Na groups. Importantly, our data also show that losartan and tempol induces a predominantly accumulation of AQP-2 in intracellular vesicles. In unanesthetized rats, Na+W group presented increased diuresis, natriuresis, and AQP-2 expression (112 ± 25 vs 64 ± 16; *p < 0.05). Water deprivation increased plasma sodium and diuresis but decreased AQP-2 (46 ± 22 vs 112 ± 25; §p < 0.05) and eNOS expression in the kidney. This study is a novel demonstration that renal endogenous Ang II–oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression.
Starting Page	465
Ending Page	478
Page Count	14
File Format	PDF
ISSN	11387548
Journal	Journal of Physiology and Biochemistry
Volume Number	70
Issue Number	2
e-ISSN	18778755
Language	English
Publisher	Springer Netherlands
Publisher Date	2014-03-04
Publisher Institution	University of Navarra, Spain
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Sodium overload Aquaporin Angiotensin II Kidney Losartan Tempol Biomedicine general Human Physiology Animal Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Medicine Biochemistry

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