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1 Pediatrics, Pharmacology and Obstetrics, Universite de Montreal, Research Center, Hopital Sainte-Justine, Montreal, Quebec, Canada
2 Institut de recherches cliniques de Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: anne-monique.nuyt{at}recherche-ste-justine.qc.ca.
In hypertension, increased peripheral vascular resistance results from vascular dysfunction with or without structural changes (vessel wall remodeling and/or microvascular rarefaction). Humans with lower birth weight exhibit evidences of vascular dysfunction. The current studies were undertaken to investigate whether in utero programming of hypertension is associated with in vivo altered response to vasoactive agents and/or abnormal vascular structure. Offspring of Wistar dams fed a normal (CTRL) or low (LP) protein isocaloric diet during gestation were studied. Mean arterial blood pressure (MABP) response to AngII was significantly increased and depressor response to sodium nitroprusside (SNP) infusions significantly decreased in male LP adult offspring relative to CTRL; response to phenylephrine infusion was not different between groups. No arterial remodeling was observed in male LP compared to CTRL offspring. Capillary and arteriolar density was significantly decreased in striated muscles from LP offspring at 7 and 28 days of life, but was not different in late fetal life (day 21 of gestation (E21)). Angiogenic potential of aortic rings from LP newborn (day of birth, P0) was significantly decreased. Striated muscle expressions (Western blots) of AngII AT1 receptor subtype, endothelial nitric oxide synthase, angiopoietin 1 and 2, Tie 2 receptor, vascular endothelial growth factor (VEGF) and receptor (VEGFR-2), and platelet derived growth factor C at E21 and P7 were unaltered by antenatal diet exposure. In conclusion, blood pressure responses to AngII and to nitric oxide donor SNP are altered and microvascular structural changes prevail in this model of fetal programming of hypertension. The capillary rarefaction is absent in the fetus and appears in the neonatal period, in association with decreased angiogenic potential. The study suggests that intra uterine protein restriction increases susceptibility to postnatal factors resulting in microvascular rarefaction which could represent a primary event in the genesis of hypertension.
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