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Role of renal sympathetic nerve activity in prenatal programming of hypertension

Authors
  • Baum, Michel1, 2
  • 1 University of Texas Southwestern Medical Center at Dallas, Department of Pediatrics, 5323 Harry Hines Building, Dallas, TX, 75390-9063, USA , Dallas (United States)
  • 2 University of Texas Southwestern Medical Center at Dallas, Department of Internal Medicine, Dallas, TX, USA , Dallas (United States)
Type
Published Article
Journal
Pediatric Nephrology
Publisher
Springer-Verlag
Publication Date
Mar 21, 2016
Volume
33
Issue
3
Pages
409–419
Identifiers
DOI: 10.1007/s00467-016-3359-8
Source
Springer Nature
Keywords
License
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Abstract

Prenatal insults, such as maternal dietary protein deprivation and uteroplacental insufficiency, lead to small for gestational age (SGA) neonates. Epidemiological studies from many different parts of the world have shown that SGA neonates are at increased risk for hypertension and early death from cardiovascular disease as adults. Animal models, including prenatal administration of dexamethasone, uterine artery ligation and maternal dietary protein restriction, result in SGA neonates with fewer nephrons than controls. These models are discussed in this educational review, which provides evidence that prenatal insults lead to altered sodium transport in multiple nephron segments. The factors that could result in increased sodium transport are discussed, focusing on new information that there is increased renal sympathetic nerve activity that may be responsible for augmented renal tubular sodium transport. Renal denervation abrogates the hypertension in programmed rats but has no effect on control rats. Other potential factors that could cause hypertension in programmed rats, such as the renin–angiotensin system, are also discussed.

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