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Related Experiment Videos

Altered vascular function in fetal programming of hypertension.

Delphine Lamireau1, Anne Monique Nuyt, Xin Hou

  • 1Research Center, Hôpital Sainte-Justine, Department of Pediatrics and Pharmacology, Université de Montréal, Montreal, Canada.

Stroke
|December 7, 2002
PubMed
Summary

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Maternal protein restriction during pregnancy leads to hypertension in offspring by impairing nitric oxide (NO)-dependent vasodilation. This dysfunction is linked to reduced soluble guanylate cyclase (sGC) expression and lower cyclic guanosine monophosphate (cGMP) levels.

Area of Science:

  • Cardiovascular Physiology
  • Developmental Programming
  • Nutritional Science

Background:

  • Chronic hypertension is often linked to reduced nitric oxide (NO) bioavailability and impaired endothelium-dependent vasodilation.
  • Intrauterine nutritional deprivation is a risk factor for hypertension and stroke, but the mechanisms behind vascular dysfunction remain unclear.

Purpose of the Study:

  • To investigate if endothelial dysfunction and altered NO-dependent vasodilation pathways are present in offspring exposed to maternal protein restriction in utero.
  • To examine the impact of in utero programming of hypertension on NO-dependent vasodilatation.

Main Methods:

  • Pregnant Wistar rats were fed diets with varying protein content (18%, 9%, or 6%).
  • Adult offspring's cerebral microvessel responses were assessed using video imaging.

Related Experiment Videos

  • Expression of endothelial nitric oxide synthase (eNOS), soluble guanylate cyclase (sGC), and K(Ca) channels was measured via Western blot.

    • Main Results:

    • Offspring from protein-restricted mothers (9% and 6% diets) exhibited significantly higher systolic blood pressure compared to controls.
    • NO-dependent vasorelaxation to substance P and acetylcholine was reduced by 50% in offspring from the low-protein group.
    • Decreased vasorelaxation to sodium nitroprusside was associated with reduced cGMP levels and sGC expression, while eNOS and K(Ca) channel function remained unchanged.

    Conclusions:

    • Maternal protein deprivation induces hypertension in offspring and impairs NO-dependent microvascular relaxation.
    • The observed vascular dysfunction is primarily attributed to decreased sGC expression and reduced cGMP levels.
    • This study offers a mechanism explaining abnormal vasorelaxation in individuals exposed to intrauterine nutritional deficits.