Article ; Online: Renal transporter activation during angiotensin-II hypertension is blunted in interferon-γ-/- and interleukin-17A-/- mice.
Hypertension (Dallas, Tex. : 1979)
2015 Volume 65, Issue 3, Page(s) 569–576
Abstract: ... IFN-γ) and interleukin-17A (IL-17A), to sodium transporter regulation in the kidney during angiotensin ... cotransporter decreased in all the 3 genotypes. Our results suggest that during Ang-II hypertension both IFN-γ ... the IL-17A(-/-) but not in IFN-γ(-/-) mice; epithelial Na channel abundance increased similarly in all the 3 ...
| Abstract | Ample genetic and physiological evidence establishes that renal salt handling is a critical regulator of blood pressure. Studies also establish a role for the immune system, T-cell infiltration, and immune cytokines in hypertension. This study aimed to connect immune cytokines, specifically interferon-γ (IFN-γ) and interleukin-17A (IL-17A), to sodium transporter regulation in the kidney during angiotensin-II (Ang-II) hypertension. C57BL/6J (wild-type) mice responded to Ang-II infusion (490 ng/kg per minute, 2 weeks) with a rise in blood pressure (170 mm Hg) and a significant decrease in the rate of excretion of a saline challenge. In comparison, mice that lacked the ability to produce either IFN-γ (IFN-γ(-/-)) or IL-17A (IL-17A(-/-)) exhibited a blunted rise in blood pressure (<150 mm Hg), and both the genotypes maintained baseline diuretic and natriuretic responses to a saline challenge. Along the distal nephron, Ang-II infusion increased abundance of the phosphorylated forms of the Na-K-2Cl cotransporter, Na-Cl cotransporter, and Ste20/SPS-1-related proline-alanine-rich kinase, in both the wild-type and the IL-17A(-/-) but not in IFN-γ(-/-) mice; epithelial Na channel abundance increased similarly in all the 3 genotypes. In the proximal nephron, Ang-II infusion significantly decreased abundance of Na/H-exchanger isoform 3 and the motor myosin VI in IL-17A(-/-) and IFN-γ(-/-), but not in wild-type; the Na-phosphate cotransporter decreased in all the 3 genotypes. Our results suggest that during Ang-II hypertension both IFN-γ and IL-17A production interfere with the pressure natriuretic decrease in proximal tubule sodium transport and that IFN-γ production is necessary to activate distal sodium reabsorption. |
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| MeSH term(s) | Angiotensin II/adverse effects ; Angiotensin II/pharmacology ; Animals ; Biological Transport/physiology ; Blood Pressure/drug effects ; Blood Pressure/physiology ; Disease Models, Animal ; Epithelial Sodium Channels/metabolism ; Genotype ; Hypertension/chemically induced ; Hypertension/metabolism ; Hypertension/physiopathology ; Interferon-gamma/deficiency ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Interleukin-17/deficiency ; Interleukin-17/genetics ; Interleukin-17/metabolism ; Kidney Tubules, Proximal/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Sodium/metabolism ; Sodium Chloride Symporters/metabolism ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/metabolism ; Solute Carrier Family 12, Member 1/metabolism | |||||
| Chemical Substances | Epithelial Sodium Channels ; Interleukin-17 ; Slc9a3 protein, mouse ; Sodium Chloride Symporters ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Solute Carrier Family 12, Member 1 ; Angiotensin II (11128-99-7) ; Interferon-gamma (82115-62-6) ; Sodium (9NEZ333N27) | |||||
| Language | English | |||||
| Publishing date | 2015-03 | |||||
| Publishing country | United States | |||||
| Document type | Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't | |||||
| ZDB-ID | 423736-5 | |||||
| ISSN | 1524-4563 ; 0194-911X ; 0362-4323 | |||||
| ISSN (online) | 1524-4563 | |||||
| ISSN | 0194-911X ; 0362-4323 | |||||
| DOI | 10.1161/HYPERTENSIONAHA.114.04975 | |||||
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| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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