Sodium retention has been proposed as the cause of hypertension in the LP rat (offspring exposed to a maternal low-protein diet in utero) model of developmental programming because of increased renal NKCC2 (Na+/K+/2Cl− co-transporter 2) expression. However, we have shown that LP rats excrete more rather than less sodium than controls, leading us to hypothesize that LP rats ingest more salt in order to maintain sodium balance. Rats were fed on either a 9% (low) or 18% (control) protein diet during pregnancy; male and female offspring were studied at 4 weeks of age. LP rats of both sexes held in metabolism cages excreted more sodium and urine than controls. When given water to drink, LP rats drank more and ate more food than controls, hence sodium intake matched excretion. However, when given a choice between saline and water to drink, the total volume of fluid ingested by LP rats fell to control levels, but the volume of saline taken was significantly larger [3.8±0.1 compared with 8.8±1.3 ml/24 h per 100 g of body weight in control and LP rats respectively; P<0.001]. Interestingly food intake also fell to control levels. Total body sodium content and ECF (extracellular fluid) volumes were greater in LP rats. These results show that prenatal programming of renal sodium wasting leads to a compensatory increase in salt appetite in LP rats. We speculate that the need to maintain salt homoeostasis following malnutrition in utero stimulates greater food intake, leading to accelerated growth and raised BP (blood pressure).
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Research Article|
November 11 2011
Prenatal programming of renal salt wasting resets postnatal salt appetite, which drives food intake in the rat
Saleh H. Alwasel;
*Fetal Programming of Diseases Research Chair, King Saud University, Riyadh 11451, Saudi Arabia
†Department of Zoology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia
Correspondence: Dr Saleh H. Alwasel (email [email protected]).
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David J. P. Barker;
David J. P. Barker
*Fetal Programming of Diseases Research Chair, King Saud University, Riyadh 11451, Saudi Arabia
‡MRC Epidemiology Resource Centre, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, U.K.
§Heart Research Center, Oregon Health and Science University, Portland, OR 97201, U.S.A.
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Nick Ashton
Nick Ashton
∥Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, U.K.
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Publisher: Portland Press Ltd
Received:
May 20 2011
Revision Received:
July 22 2011
Accepted:
October 03 2011
Accepted Manuscript online:
October 03 2011
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2012 Biochemical Society
2012
Clin Sci (Lond) (2012) 122 (6): 281–288.
Article history
Received:
May 20 2011
Revision Received:
July 22 2011
Accepted:
October 03 2011
Accepted Manuscript online:
October 03 2011
Connected Content
A correction has been published:
Prenatal programming of renal salt wasting resets postnatal salt appetite, which drives food intake in the rat
Citation
Saleh H. Alwasel, David J. P. Barker, Nick Ashton; Prenatal programming of renal salt wasting resets postnatal salt appetite, which drives food intake in the rat. Clin Sci (Lond) 1 March 2012; 122 (6): 281–288. doi: https://doi.org/10.1042/CS20110266
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