High‐salt intake reduces renal tissue levels of inflammatory cytokines in mice

High salt (HS) intake is usually considered as an aggravating factor to induce inflammatory renal injury. However, the changes in the renal levels of inflammatory cytokines during HS intake is not yet clearly defined. We hypothesize that HS increases renal levels of tumor necrosis factor‐alpha (TNF‐...

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Veröffentlicht in:Physiological reports 2021-01, Vol.8 (24), p.e14621-n/a
Hauptverfasser: Singh, Purnima, Stephenson, Roxan, Castillo, Alexander, Majid, Dewan S. A.
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Sprache:eng
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Zusammenfassung:High salt (HS) intake is usually considered as an aggravating factor to induce inflammatory renal injury. However, the changes in the renal levels of inflammatory cytokines during HS intake is not yet clearly defined. We hypothesize that HS increases renal levels of tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6) but decreases interleukin‐10 (IL‐10; anti‐inflammatory cytokine) and these responses exacerbate in NO deficient conditions. Both wild‐type (WT) and endothelial NO synthase knockout (eNOSKO) mice (~8 weeks old, n = 6 in each group) were given normal‐salt (NS; 0.3% NaCl) and HS (4% NaCl) containing diets for 2 weeks. Systolic blood pressure (SBP) was determined by tail‐cuff plethysmography and urine collections were made using metabolic cages. Basal SBP was higher in eNOSKO than WT mice (131 ± 7 vs 117 ± 3 mmHg; p 
ISSN:2051-817X
DOI:10.14814/phy2.14621