Prenatal hypoxia leads to hypertension, renal renin-angiotensin system activation and exacerbates salt-induced pathology in a sex-specific manner
SL Walton, H Bielefeldt-Ohmann, RR Singh, J Li, TM Paravicini, MH Little, KM Moritz
SCIENTIFIC REPORTS | NATURE PUBLISHING GROUP | Published : 2017
Prenatal hypoxia is associated with growth restriction and adverse cardiovascular outcomes. Here, we describe renal and cardiovascular outcomes in ageing mouse offspring prenatally exposed to hypoxia (12% O2) from embryonic day 14.5 until birth. At 12 months of age, both male and female offspring exposed to prenatal hypoxia had elevated mean arterial pressure. Glomerular number was reduced by 25% in hypoxia-exposed male, but not female, offspring and this was associated with increased urinary albumin excretion, glomerular hypertrophy and renal fibrosis. Hypoxia-exposed offspring of both sexes were more susceptible to salt-induced cardiac fibrosis, however, renal fibrosis was exacerbated by h..View full abstract
Awarded by National Health and Medical Research Council of Australia
We thank Kym French and Sarah Steane for their technical support to this work. This project was funded by the National Health and Medical Research Council of Australia (NHMRC-APP1009338). K.M.M. was supported by fellowships provided by the NHMRC. S.L.W. was supported by an Australian Postgraduate Award.