Background Low birth weight is associated with an increased risk of adult cardiovascular disease. The concept of “fetal programming” of disease has been supported by animal models, which have shown that the restriction of maternal substrates induces intrauterine growth restriction (IUGR), later elevated blood pressure and vascular dysfunction. Nitric oxide (NO) is one of the primary modulators of vascular tone. Defects in the NO pathway have been implicated in various vascular pathological states. The aim of our study was to test the influence of IUGR on endothelial function, particularly the NO-dependent vasodilation pathway.
Methods Pregnant rats were fed either a control (22% casein) or protein-restricted (9% casein) diet during gestation. Endothelium-intact aortic rings of young male offspring (5–6 weeks) of the control and IUGR groups were isolated. The vascular reactivity was tested with dose–response curves to the endothelium-dependent dilator acetylcholine and the endothelium-independent dilator sodium nitroprusside (SNP) before the occurrence of systemic arterial hypertension.
Results The birth weight was lower in the IUGR group than the control group (5.78 ± 0.5 g vs 6.69 ± 0.4 g, respectively, p<0.01). Aortic rings of the offsprings in the IUGR group showed decreased responses to phenylephrine (−46%, p<0.5) and decreased vasodilation to acetylcholine (−20%, p<0.5) in comparison with aortic rings of the control group, although the vasodilation response to the NO donor SNP was similar in the two groups.
Conclusion Endothelium-dependent vascular relaxation is reduced in the aorta from IUGR. Defects in the NO-dependent vasodilation pathway in IUGR may be suggested.