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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2006-10-6
pubmed:abstractText
The aim of the present study was to determine whether acute sodium overload could trigger an inflammatory reaction in the tubulointerstitial (TI) compartment in normal rats. Four groups of Sprague-Dawley rats received increasing NaCl concentrations by intravenous infusion. Control (C): Na+ 0.15 M; G1: Na+ 0.5 M; G2: Na+ 1.0 M; and G3: Na+ 1.5 M. Creatinine clearance, mean arterial pressure (MAP), renal blood flow (RBF), and sodium fractional excretion were determined. Transforming growth factor beta1 (TGF-beta1), alpha-smooth muscle actin (alpha-SMA), RANTES, transcription factor nuclear factor-kappa B (NF-kappaB), and angiotensin II (ANG II) were evaluated in kidneys by immunohistochemistry. Animals with NaCl overload showed normal glomerular function without MAP and RBF modifications and exhibited a concentration-dependent natriuretic response. Plasmatic sodium increased in G2 (P < 0.01) and G3 (P < 0.001). Light microscopy did not show renal morphological damage. Immunohistochemistry revealed an increased number of ANG II-positive tubular cells in G2 and G3, and positive immunostaining for NF-kappaB only in G3 (P < 0.01). Increased staining of alpha-SMA in the interstitium (P < 0.01), TGF-beta1 in tubular cells (P < 0.01), and a significant percentage (P < 0.01) of positive immunostaining for RANTES in tubular epithelium and in glomerular and peritubular endothelium were detected in G3 > G2 > C group. These results suggest that an acute sodium overload is able 'per se' to initiate TI endothelial inflammatory reaction (glomerular and peritubular) and incipient fibrosis in normal rats, independently of hemodynamic modifications. Furthermore, these findings are consistent with the possibility that activation of NF-kappaB and local ANG II may be involved in the pathway of this inflammatory process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1439-46
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16955102-Actins, pubmed-meshheading:16955102-Angiotensin II, pubmed-meshheading:16955102-Animals, pubmed-meshheading:16955102-Biological Transport, pubmed-meshheading:16955102-Blood Pressure, pubmed-meshheading:16955102-Cell Respiration, pubmed-meshheading:16955102-Chemokine CCL5, pubmed-meshheading:16955102-Dose-Response Relationship, Drug, pubmed-meshheading:16955102-Immunohistochemistry, pubmed-meshheading:16955102-Inflammation, pubmed-meshheading:16955102-Kidney Tubules, pubmed-meshheading:16955102-Male, pubmed-meshheading:16955102-NF-kappa B, pubmed-meshheading:16955102-Nephritis, Interstitial, pubmed-meshheading:16955102-Rats, pubmed-meshheading:16955102-Rats, Sprague-Dawley, pubmed-meshheading:16955102-Regional Blood Flow, pubmed-meshheading:16955102-Sodium, pubmed-meshheading:16955102-Transforming Growth Factor beta, pubmed-meshheading:16955102-Transforming Growth Factor beta1
pubmed:year
2006
pubmed:articleTitle
Acute sodium overload produces renal tubulointerstitial inflammation in normal rats.
pubmed:affiliation
Cátedras de Fisiopatología Farmacologia Bioquímica Clínica y Anatomía Macro y Microscópica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Piso, Buenos Aires. iroson@ffyb.uba.ar
pubmed:publicationType
Journal Article