Normal lactational environment restores nephron endowment and prevents hypertension after placental restriction in the rat

Wlodek, Mary E., Mibus, Amy, Tan, Adeline, Siebel, Andrew L., Owens, Julie A. and Moritz, Karen M. 2007, Normal lactational environment restores nephron endowment and prevents hypertension after placental restriction in the rat, Journal of the American Society of Nephrology, vol. 18, no. 6, pp. 1688-1696, doi: 10.1681/ASN.2007010015.

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Title Normal lactational environment restores nephron endowment and prevents hypertension after placental restriction in the rat
Author(s) Wlodek, Mary E.
Mibus, Amy
Tan, Adeline
Siebel, Andrew L.
Owens, Julie A.ORCID iD for Owens, Julie A. orcid.org/0000-0002-7498-1353
Moritz, Karen M.
Journal name Journal of the American Society of Nephrology
Volume number 18
Issue number 6
Start page 1688
End page 1696
Total pages 9
Publisher American Society of Nephrology
Place of publication Gainesville, Fla.
Publication date 2007-06
ISSN 1046-6673
Keyword(s) Animals
Animals, Suckling
Birth Weight
Blood Pressure
Female
Fetal Growth Retardation
Hypertension, Renal
Kidney Glomerulus
Lactation
Litter Size
Male
Milk
Nephrons
Organ Size
Pregnancy
Prenatal Exposure Delayed Effects
RNA, Messenger
Rats
Rats, Inbred WKY
Receptor, Angiotensin, Type 1
Science & Technology
Life Sciences & Biomedicine
Urology & Nephrology
MATERNAL PROTEIN RESTRICTION
RENIN-ANGIOTENSIN SYSTEM
ADULT-BLOOD PRESSURE
INTRAUTERINE GROWTH RESTRICTION
BIRTH-WEIGHT
GENE-EXPRESSION
RECEPTOR EXPRESSION
CHILDHOOD GROWTH
UTEROPLACENTAL INSUFFICIENCY
CARDIOVASCULAR-DISEASE
Summary Uteroplacental insufficiency in the rat restricts fetal growth, impairs mammary development, compromising postnatal growth; and increases adult BP. The roles of prenatal and postnatal nutritional restraint on later BP and nephron endowment in offspring from mothers that underwent bilateral uterine vessel ligation (restricted) on day 18 of pregnancy were examined. Sham surgery (control) and a group of rats with reduced litter size (reduced; litter size reduced at birth to five, equivalent to restricted group) were used as controls. Offspring (control, reduced, and restricted) were cross-fostered on postnatal day 1 onto a control (normal lactation) or restricted (impaired lactation) mother. BP in male offspring was determined by tail cuff at 8, 12, and 20 wk of age, with glomerular number and volume (Cavalieri/Physical Dissector method) and renal angiotensin II type 1 receptor (AT(1)R) mRNA expression (real-time PCR) determined at 6 mo. Restricted-on-restricted male offspring developed hypertension (+16 mmHg) by 20 wk together with a nephron deficit (-26%) and glomerular hypertrophy (P < 0.05). In contrast, providing a normal lactational environment to restricted offspring improved postnatal growth and prevented the nephron deficit and hypertension. Reduced-on-restricted pups that were born of normal weight but with impaired growth during lactation subsequently grew faster, developed hypertension (+16 mmHg), had increased AT(1A)R and AT(1B)R mRNA expression (P < 0.05), but had no nephron deficit. Our study identifies the prenatal and postnatal nutritional environments in the programming of adult hypertension, associated with distinct renal changes. It is shown for the first time that a prenatally induced nephron deficit can be restored by correcting growth restriction during lactation.
Language eng
DOI 10.1681/ASN.2007010015
Field of Research 1103 Clinical Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2007, American Society of Nephrology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30116763

Document type: Journal Article
Collection: Office of the Deputy Vice-Chancellor (Research)
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