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Maternal hypomagnesemia alters renal function but does not program changes in the cardiovascular physiology of adult offspring

Part of: DOHaD ANZ Conference 2015

Published online by Cambridge University Press:  28 March 2016

R. N. Schlegel ,
K. M. Moritz  and
T. M. Paravicini
R. N. Schlegel
Affiliation:
School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia
K. M. Moritz
Affiliation:
School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia
T. M. Paravicini*
Affiliation:
School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia School of Medical Sciences, RMIT University, Melbourne, VIC, Australia
*
*Address for correspondence: T. Paravicini, School of Medical Sciences, RMIT University, Bundoora, VIC 3083, Australia. (Email [email protected])
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Abstract

Maternal undernutrition is known to adversely impact fetal health and development. Insults experienced in utero alter development of the fetus as it adapts to microenvironment stressors, leading to growth restriction and subsequent low birth weight. Infants born small for gestational age have significantly increased risk of developing cardiovascular and renal disease in later life, an effect that is often characterized by hypertension and reduced glomerular number. Maternal magnesium (Mg2+) deficiency during pregnancy impairs fetal growth, however, the long-term health consequences for the offspring remain unknown. Here, we used a mouse model of dietary Mg2+ deficiency before and during pregnancy to investigate cardiovascular and renal outcomes in male and female adult offspring at 6 months of age. There were no differences between groups in 24-h mean arterial pressure or heart rate as measured by radiotelemetry. Cardiovascular responses to aversive (restraint, dirty cage switch) and non-aversive (feeding response) stressors were also similar in all groups. There were no differences in nephron number, however, Mg2+-deficient offspring had increased urine flow (in both males and females) and reduced Mg2+ excretion (in males only). Despite evidence suggesting that maternal nutrient restriction programs for hypertension in adult offspring, we found that a moderate level of maternal dietary Mg2+ deficiency did not program for a nephron deficit, or alter cardiovascular function at 6 months of age. These data suggest there are no long-term adverse outcomes for the cardiovascular health of offspring of Mg2+ deficient mothers.

Keywords

Blood pressuremagnesiumnephron number
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 7 , Issue 5: Themed Issue: Australia/New Zealand 2015 DOHaD Scientific Meeting: Advances and Updates , October 2016 , pp. 473 - 480
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Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2016 

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