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Plos One : Perinatal Na+ Overload Programs Raised Renal Proximal Na+ Transport and Enalapril-sensitive Alterations of Ang II Signaling Pathways During Adulthood, Volume 7

By Ashton, Nick

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Book Id: WPLBN0003958124
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Perinatal Na+ Overload Programs Raised Renal Proximal Na+ Transport and Enalapril-sensitive Alterations of Ang II Signaling Pathways During Adulthood, Volume 7  
Author: Ashton, Nick
Volume: Volume 7
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection
Historic
Publication Date:
Publisher: Plos

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Ashton, N. (n.d.). Plos One : Perinatal Na+ Overload Programs Raised Renal Proximal Na+ Transport and Enalapril-sensitive Alterations of Ang II Signaling Pathways During Adulthood, Volume 7. Retrieved from http://netlibrary.net/


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Description : Background : High Na+ intake is a reality in nowadays and is frequently accompanied by renal and cardiovascular alterations. In this study, renal mechanisms underlying perinatal Na+ overload-programmed alterations in Na+ transporters and the renin/angiotensin system (RAS) were investigated, together with effects of short-term treatment with enalapril in terms of reprogramming molecular alterations in kidney. Methodology/Principal Findings : Male adult Wistar rats were obtained from dams maintained throughout pregnancy and lactation on a standard diet and drinking water (control) or 0.17 M NaCl (saline group). Enalapril (100 mg/l), an angiotensin converting enzyme inhibitor, was administered for three weeks after weaning. Ninety day old offspring from dams that drank saline presented with proximal tubules exhibiting increased (Na++K+)ATPase expression and activity. Ouabaininsensitive Na+-ATPase activity remained unchanged but its response to angiotensin II (Ang II) was lost. PKC, PKA, renal thiobarbituric acid reactive substances (TBARS), macrophage infiltration and collagen deposition markedly increased, and AT2 receptor expression decreased while AT1 expression was unaltered. Early treatment with enalapril reduced expression and activity of (Na++K+)ATPase, partially recovered the response of Na+-ATPase to Ang II, and reduced PKC and PKA activities independently of whether offspring were exposed to high perinatal Na+ or not. In addition, treatment with enalapril per se reduced AT2 receptor expression, and increased TBARS, macrophage infiltration and collagen deposition. The perinatally Na+-overloaded offspring presented high numbers of Ang II-positive cortical cells, and significantly lower circulating Ang I, indicating that programming/reprogramming impacted systemic and local RAS. Conclusions/Significance : Maternal Na+ overload programmed alterations in renal Na+ transporters and in its regulation, as well as severe structural lesions in adult offspring. Enalapril was beneficial predominantly through its influence on Na+ pumping activities in adult offspring. However, side effects including down-regulation of PKA, PKC and AT2 receptors and increased TBARS could impair renal function in later life.

 

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