Background:

The heritability of salt-sensitive hypertension and the heightened susceptibility of offspring to maternal perinatal high salt diet (HSD) indicate that hypertension may originate early in life. However, the mechanism underlying this phenomenon remains unclear. We hypothesized that perinatal exposure of dams to HSD will increase inflammation, impair vascular function and elevate blood pressure (BP) in the adult offspring.

Methods:

Pregnant rats were fed a normal (0.3%) or high (8%) salt diet during pregnancy and the offspring from each group were weaned at 4 weeks of age and placed on normal salt diet (NSD) for 12 weeks. BP measurement, vascular reactivity studies, and ELISA assay for C-reactive proteins (CRP), Tumor Necrotic Factor (TNF-α), and Interleukin-6 (IL-6) were carried out. Data were analyzed using student t-test. The significance level was set at P-values ⩽.05.

Results:

The offspring of dams exposed to perinatal HSD exhibited elevated BP parameters compared to those from dams on NSD. Although the maximum contractile response to noradrenaline was similar in both groups (P > .05), the maximum relaxation response to acetylcholine was significantly reduced in offspring of HSD-exposed dams (P < .01), indicating impaired endothelial function. Furthermore, perinatal HSD led to increased levels of CRP, TNF-α, and IL-6 in the offspring, indicating heightened systemic and vascular inflammation.

Conclusion:

Findings from this study show that maternal perinatal HSD increased biomarkers of inflammation, impaired endothelial function and elevated BP in the adult offspring. These findings suggest maternal perinatal consumption of high dietary salt renders the offspring more susceptible to hypertension in adulthood.

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Perinatal Exposure of Dams to a High Salt Diet Impaired Vascular Function and Elevated Biomarkers of Inflammation in the Offspring