PMID- 16955102
OWN - NLM
STAT- MEDLINE
DCOM- 20061107
LR  - 20131121
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 70
IP  - 8
DP  - 2006 Oct
TI  - Acute sodium overload produces renal tubulointerstitial inflammation in normal 
      rats.
PG  - 1439-46
AB  - 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.
FAU - Roson, M I
AU  - Roson MI
AD  - Catedras de Fisiopatologia Farmacologia Bioquimica Clinica y Anatomia Macro y 
      Microscopica, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, 
      Piso, Buenos Aires. iroson@ffyb.uba.ar
FAU - Cavallero, S
AU  - Cavallero S
FAU - Della Penna, S
AU  - Della Penna S
FAU - Cao, G
AU  - Cao G
FAU - Gorzalczany, S
AU  - Gorzalczany S
FAU - Pandolfo, M
AU  - Pandolfo M
FAU - Kuprewicz, A
AU  - Kuprewicz A
FAU - Canessa, O
AU  - Canessa O
FAU - Toblli, J E
AU  - Toblli JE
FAU - Fernandez, B E
AU  - Fernandez BE
LA  - eng
PT  - Journal Article
DEP - 20060906
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Actins)
RN  - 0 (Chemokine CCL5)
RN  - 0 (NF-kappa B)
RN  - 0 (Tgfb1 protein, rat)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (smooth muscle actin, rat)
RN  - 11128-99-7 (Angiotensin II)
RN  - 9NEZ333N27 (Sodium)
SB  - IM
MH  - Actins/metabolism
MH  - Angiotensin II/metabolism
MH  - Animals
MH  - Biological Transport/physiology
MH  - Blood Pressure/drug effects
MH  - Cell Respiration/physiology
MH  - Chemokine CCL5/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Immunohistochemistry
MH  - Inflammation/physiopathology
MH  - Kidney Tubules/blood supply/drug effects/metabolism/*pathology
MH  - Male
MH  - NF-kappa B/metabolism
MH  - Nephritis, Interstitial/*etiology/metabolism/*pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Regional Blood Flow/drug effects
MH  - Sodium/*adverse effects/metabolism
MH  - Transforming Growth Factor beta/metabolism
MH  - Transforming Growth Factor beta1
EDAT- 2006/09/07 09:00
MHDA- 2006/11/09 09:00
CRDT- 2006/09/07 09:00
PHST- 2006/09/07 09:00 [pubmed]
PHST- 2006/11/09 09:00 [medline]
PHST- 2006/09/07 09:00 [entrez]
AID - S0085-2538(15)52171-6 [pii]
AID - 10.1038/sj.ki.5001831 [doi]
PST - ppublish
SO  - Kidney Int. 2006 Oct;70(8):1439-46. doi: 10.1038/sj.ki.5001831. Epub 2006 Sep 6.