Uteroplacental insufficiency causes a nephron deficit, modest renal insufficiency but no hypertension with ageing in female rats

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dc.contributor.authorMoritz, K.
dc.contributor.authorMazzuca, M.
dc.contributor.authorSiebel, A.
dc.contributor.authorMibus, A.
dc.contributor.authorArena, D.
dc.contributor.authorTare, M.
dc.contributor.authorOwens, J.
dc.contributor.authorWlodek, M.
dc.date.issued2009
dc.description.abstractIn rats, uteroplacental insufficiency induced by uterine vessel ligation restricts fetal growth and impairs mammary development compromising postnatal growth. In male offspring, this results in a nephron deficit and hypertension which can be reversed by improving lactation and postnatal growth. Here, growth, blood pressure and nephron endowment in female offspring from mothers which underwent bilateral uterine vessel ligation (Restricted) on day 18 of pregnancy were examined. Sham surgery (Control) and a reduced litter group (Reduced at birth to 5, equivalent to Restricted group) were used as controls. Offspring (Control, Reduced, Restricted) were cross-fostered on postnatal day 1 onto a Control (normal lactation) or Restricted (impaired lactation) mother. Restricted-on-Restricted offspring were born small but were of similar weight to Control-on-Control by postnatal day 35. Blood pressure was not different between groups at 8, 12 or 20 weeks of age. Glomerular number was reduced in Restricted-on-Restricted offspring at 6 months without glomerular hypertrophy. Cross-fostering a Restricted pup onto a Control dam resulted in a glomerular number intermediate between Control-on-Control and Restricted-on-Restricted. Blood pressure, along with renal function, morphology and mRNA expression, was examined in Control-on-Control and Restricted-on-Restricted females at 18 months. Restricted-on-Restricted offspring did not become hypertensive but developed glomerular hypertrophy by 18 months. They had elevated plasma creatinine and alterations in renal mRNA expression of transforming growth factor-β1, collagen IV (α1) and matrix matelloproteinase-9. This suggests that perinatally growth restricted female offspring may be susceptible to onset of renal injury and renal insufficiency with ageing in the absence of concomitant hypertension.
dc.description.statementofresponsibilityKaren M. Moritz, Marc Q. Mazzuca, Andrew L. Siebel, Amy Mibus, Debbie Arena, Marianne Tare, Julie A. Owens and Mary E. Wlodek
dc.identifier.citationThe Journal of Physiology, 2009; 587(11):2635-2646
dc.identifier.doi10.1113/jphysiol.2009.170407
dc.identifier.issn0022-3751
dc.identifier.issn1469-7793
dc.identifier.orcidOwens, J. [0000-0002-7498-1353]
dc.identifier.urihttp://hdl.handle.net/2440/54926
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.source.urihttps://doi.org/10.1113/jphysiol.2009.170407
dc.subjectUterus
dc.subjectKidney Glomerulus
dc.subjectAnimals
dc.subjectRats, Inbred WKY
dc.subjectRats
dc.subjectFetal Growth Retardation
dc.subjectPlacental Insufficiency
dc.subjectDisease Models, Animal
dc.subjectBirth Weight
dc.subjectCreatinine
dc.subjectExtracellular Matrix Proteins
dc.subjectOrgan Size
dc.subjectLigation
dc.subjectAge Factors
dc.subjectSex Factors
dc.subjectGene Expression Regulation
dc.subjectWater-Electrolyte Balance
dc.subjectAging
dc.subjectGestational Age
dc.subjectLactation
dc.subjectPregnancy
dc.subjectLitter Size
dc.subjectBlood Pressure
dc.subjectFemale
dc.subjectRenal Insufficiency
dc.titleUteroplacental insufficiency causes a nephron deficit, modest renal insufficiency but no hypertension with ageing in female rats
dc.typeJournal article
pubs.publication-statusPublished

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