Prenatal hypoxia leads to hypertension, renal renin-angiotensin system activation and exacerbates salt-induced pathology in a sex-specific manner.

Perivascular fibrosis area tended to be greater in male hypoxia-exposed offspring, with no effect of HS, although this did not reach statistical significance (control NS: 2.2 ± 0.6, hypoxia NS: 3.6 ± 0.9, control HS: 2.4 ± 0.2, hypoxia HS: 3.2 ± 0.4; P treatment = 0.08, P diet = 0.8).

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