Maternal food restriction in the second half of pregnancy affects vascular function but not blood pressure of rat female offspring

Abstract

Food restriction during pregnancy in rats induces intrauterine growth retardation with consequences persisting into adulthood. In the present study we have investigated the hypothesis that malnutrition in pregnant rats may lead to altered cardiovascular function in adult female offspring. Perinatal growth retardation was induced by a 50 % reduction of normal dietary intake in rats during the second half of pregnancy. Systolic and diastolic blood pressure values and heart rate were recorded in conscious female offspring (100 d old) using a femoral artery probe. No significant differences in heart rate, or in systolic and diastolic blood pressures were recorded between control offspring and offspring of nutritionally deprived rats. In order to ascertain whether cardiovascular variables in the offspring were influenced by lactation, subgroups of offspring from food-restricted dams were fostered with lactating dams fed on a normal diet. Blood pressure and heart rate were also found to be normal in these offspring. The rise in blood pressure associated with NO inhibition was similar in all groups. Isolated resistance artery function was assessed in vitro in offspring (100-120 d old) of a second group of semistarved dams. Small mesenteric arteries from these animals showed reduced endotheliumdependent relaxation (to acetylcholine and bradykinin), but enhanced sensitivity to exogenous NO (sodium nitroprusside). We conclude that food restriction during the second half of pregnancy and/or lactation does not induce hypertension in adult offspring, but may effect subtle changes in vascular function.

Nephron endowment and blood pressure: What do we really know?

“…Despite similar growth retardation, glomerular number and blood pressure of female littermates were unaffected by IUGR [26]. These findings suggest that sex might provide protection against renal insult with some interventions, but also confirm previous findings that IUGR, or, indeed, low birth weight, does not always lead to reductions in glomerular number or hypertension [27,28].…”

Chronic moderate hypoxia during in ovo development alters arterial reactivity in chickens

“…In the present study the data obtained after L-NAME application suggest that in ovo chronic hypoxia can reduce the release of NO. Decreased arterial endothelial function as a result of chronic hypoxemia has been described to occur in the mammalian fetus [25,42] and in rats that were exposed to maternal food restriction during the second half of gestation [16]. However, this vascular dysfunction has not been studied postnatally in systemic arteries of animals that were exposed to chronic hypoxia insult in utero.…”

Adult cardiorenal benefits from postnatal fish oil supplement in rat offspring of low-protein pregnancies

“…In the different protein restriction protocols studied birth weight is usually reduced (Holemans et al, 1999;Vickers et al, 2001;Woods et al, 2001). However, an increase in birth weight (LangleyEvans et al, 1996b) or no effect (Langley and Jackson, 1994) resulting from maternal protein restriction have been reported.…”