Skip Navigation



NDT Advance Access published online on September 16, 2005
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfi133
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
20/12/2654    most recent
gfi133v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Bento, L. M. A.
Right arrow Articles by Gontijo, J. A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bento, L. M. A.
Right arrow Articles by Gontijo, J. A. R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received February 10, 2005
Accepted August 12, 2005

Original Articles

Effects of NH4Cl intake on renal growth in rats: role of MAPK signalling pathway

Leda M. A. Bento 1, Jose B. C. Carvalheira 2, Leonardo F. Menegon 1, Mario J. A. Saad 2, and Jose A. R. Gontijo 1*

1 Laboratórios de Metabolismo Hidro-Salino e, Universidade Estadual de Campinas, Campinas, SP, Brazil
2 Biologia Molecular, Departamento de Clinica Médica, Núcleo de Medicina e Cirurgia Experimental, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, SP, Brazil

* To whom correspondence should be addressed.
Jose A. R. Gontijo, E-mail: gontijo{at}fcm.unicamp.br



  Abstract

Background. There is a surprising lack of experimental data on the mechanisms of NH4Cl-induced chronic metabolic acidosis which causes kidney hypertrophy. The NH4Cl treatment results in an absolute increase in kidney mass. Despite findings to indicate a close interaction between NH4Cl-induced chronic metabolic acidosis and renal enlargement, the role of the stimulated serine kinase cascade, mediated by the stepwise activation of extracellular signal-regulated kinase (ERK) signalling, on kidney hypertrophy has not yet been investigated.

Methods. To test this hypothesis, the present study was undertaken to further explore the possible involvement of mitogen-activated protein kinase (MAPK) signalling pathway in renal growth in chronic NH4Cl-treated rats by western blot analysis.

Results. Our major findings are as follows: (1) Urinary sodium excretion significantly increased during the early phases of NH4Cl-induced acidosis, (2) This occurrence is associated with sustained renal hypertrophy, and (3) sustained basal phosphorylation of IRS-1, Shc, and MAPK/ERKs in acidotic kidneys.

Conclusions. The present study confirms that NH4Cl-induced acidosis causes disturbances in renal sodium handling. In addition, these findings demonstrate a sustained pre-stimuli activation of kidney MAPK/ERKs signalling pathways in the NH4Cl-treated rats that may correlate with an increased rate of kidney hypertrophy and a transient renal tubule inability to handle sodium. Thus, the altered renal electrolyte handling may result from a reciprocal relationship between the level of renal tubule metabolic activity and ion transport. In addition, the study shows that the appropriate regulation of tyrosine kinase protein phosphorylation, and its downstream signal transduction pathway, plays an important role on renal growth in the NH4Cl-treated rats.

Keywords: IRS-1; kidney growth; MAPK/ERK; metabolic acidosis; NH4Cl; Shc; sodium excretion.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
F. F. Mesquita, J. A. R. Gontijo, and P. A. Boer
Expression of renin-angiotensin system signalling compounds in maternal protein-restricted rats: effect on renal sodium excretion and blood pressure
Nephrol. Dial. Transplant., September 30, 2009; (2009) gfp505v1.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
L. M. A. Bento, M. M. Fagian, A. E. Vercesi, and J. A. R. Gontijo
Effects of NH4Cl-induced systemic metabolic acidosis on kidney mitochondrial coupling and calcium transport in rats
Nephrol. Dial. Transplant., October 1, 2007; 22(10): 2817 - 2823.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
R. Pedrosa, N. Goncalves, U. Hopfer, P. A. Jose, and P. Soares-da-Silva
Activity and Regulation of Na+-HCO3- Cotransporter in Immortalized Spontaneously Hypertensive Rat and Wistar-Kyoto Rat Proximal Tubular Epithelial Cells
Hypertension, May 1, 2007; 49(5): 1186 - 1193.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.