The effects of anaemia on heart, placenta and body weight, and blood pressure in fetal and neonatal rats.

Crowe, Catherine; Dandekar, Pramila V.; Fox, María Ofelia Barber; Dhingra, Kapil; Bennet, Laura; Hanson, Mark A.

doi:10.1113/jphysiol.1995.sp020986

Cited by 97 publications

(95 citation statements)

References 14 publications

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“…The enlarged hearts in the PID animals during the neonatal period are consistent with reports by others 5,7,9,22 and may be an adaptive response to anemia during gestation and the neonatal periods. Indeed, fetal anemia has been shown to increase heart weight and cardiac output in sheep.…”

Section: Discussionsupporting

confidence: 91%

“…Specifically, studies in rats have shown that inadequate iron supply during early development can produce hypertension, even when iron levels are subsequently normalized. [5][6][7][8][9][10] In fact, Lisle et al 8 demonstrated that PID produced both a nephron deficit and elevated blood pressure in adult offspring. Although the effects of PID on renal function were not investigated, the study by Lisle et al 8 implicates the developing kidney as a potential target for perinatal insult.…”

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confidence: 99%

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Long-Term Circulatory Consequences of Perinatal Iron Deficiency in Male Wistar Rats

et al. 2008

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Abstract-Perinatal iron deficiency (PID) has been reported to induce developmental abnormalities, including cardiovascular complications in rats. These complications are believed to be "programmed" by an aberrant perinatal environment because the changes persist long after the insult is corrected (ie, despite subsequent iron replenishment). Little is known about the mechanisms by which PID affects blood pressure in the offspring, although the kidney is likely to play a central role. The objective of this study was to investigate the circulatory complications of PID and the putative role of the kidney involved therein. Before and throughout gestation, female Wistar rats were fed either a low-iron diet (3 ppm/10 ppm Fe) or an iron-enriched diet (225 ppm Fe). After giving birth, all of the dams were placed on a standard grain-based diet. At 24 hours postpartum, hematocrits and hemoglobin levels from offspring of iron-deficient mothers were 60% and 59% of control values, respectively. Adult PID animals had greater mean arterial pressures (110 versus 106 mm Hg) and systolic blood pressures (129 versus124 mm Hg) than controls, as assessed by radiotelemetry. The relationship between renal arterial pressure and renal interstitial hydrostatic pressure, assessed in anesthetized rats, was blunted by 41% in the PID group compared with controls. In addition, arterial pressure changes were significantly greater in response to altered sodium in the PID animals compared with controls. These data confirm that PID adversely affects blood pressure control, which seems to be mediated, at least in part, by altered intrarenal hemodynamic properties.

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Section: Discussionsupporting

confidence: 91%

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confidence: 99%

Long-Term Circulatory Consequences of Perinatal Iron Deficiency in Male Wistar Rats

et al. 2008

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“…Surprisingly, Pcm mutant animals exhibited a severe iron deficiency at birth, more severe in homozygotes (Mok et al, 2004). Because fetal iron and other nutrient requirements are met by placental transport from the maternal to fetal blood circulation, maternal Development 131 (19) Research article iron deficiency exerts profound effects on fetal as well as postnatal development (Crowe et al, 1995) (for a review, see McArdle et al, 2003). Interestingly, fetuses exhibit decreased severity of iron deficiency in comparison to the mother, indicating the presence of regulatory mechanisms to sustain an adequate supply of iron to the fetus (Gambling et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

et al. 2004

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Regulatory interferences at the iron transporter ferroportin 1 (Fpn1) cause transient defects in iron homeostasis and erythropoiesis in polycythaemia(Pcm) mutant mice. The present study identified decreased Fpn1 expression in placental syncytiotrophoblast cells at late gestation as the mechanism of neonatal iron deficiency in Pcm mutants. Tissue specificity of embryonic Fpn1 dysregulation was evident from concomitant decreases in Fpn1 mRNA and protein expression in placenta and liver, as opposed to upregulation of Fpn1 protein despite decreased transcript levels in spleen, implicating post-transcriptional regulation of Fpn1. Dysregulation of Fpn1 and decreased iron levels in Pcm mutant spleens correlated with apoptotic cell death in the stroma, resulting in a semidominant spleen regression. At 7 weeks of age, a transient increase in spleen size in Pcm heterozygotes reflected a transient erythropoietin-mediated polycythemia. Structurally, Pcm mutant spleens displayed a severe defect in red pulp formation, including disruption of the sinusoidal endothelium, as well as discrete defects in white pulp organization during postnatal development. Reduced functional competence of the Pcmmutant spleen was manifested by an impaired response to chemically induced hemolytic anemia. Thus, aberrant Fpn1 regulation and iron homeostasis interferes with development of the spleen stroma during embryogenesis,resulting in a novel defect in spleen architecture postnatally.

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“…Undernutrition in pregnancy results in IUGR and high BP in adult life in sheep (65), rats (86), and guinea pigs (40) and a reduced life span in rats (4,149). Fetal hypoxia, induced by unilateral uterine artery ligation in guinea pigs (115), aortic ligation in rats (5), uterine artery ligation in rats (70), removal of endometrial caruncles in sheep (125), maternal hypobaric hypoxia in rats (151), and iron deficiency anemia in rats (32,95) are also associated with IUGR and hypertension later in life. Together, these observations point at metabolism and oxygen supply as central factors.…”

Section: Experimental Evidence Of Programmingmentioning

confidence: 99%

Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon

Racasan¹,

Braam²,

Koomans³

et al. 2005

American Journal of Physiology-Renal Physiology

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Racasan, Simona, Branko Braam, Hein A. Koomans, and Jaap A. Joles. Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon. Am J Physiol Renal Physiol 288: F626 -F636, 2005. First published November 16, 2004 doi:10.1152/ ajprenal.00314.2004.-The "programming hypothesis" proposes that an adverse perinatal milieu leads to adaptation that translates into cardiovascular disease in adulthood. The balance between nitric oxide (NO) and reactive oxygen species (ROS) is disturbed in cardiovascular diseases, including hypertension. Conceivably, this balance is also disturbed in pregnancy, altering the fetal environment; however, effects of perinatal manipulation of NO and ROS on adult blood pressure (BP) are unknown. In spontaneously hypertensive rats (SHR), NO availability is decreased and ROS are increased compared with normotensive Wistar-Kyoto rats, and, despite the genetic predisposition, the perinatal environment can modulate adult BP. Our hypothesis is that a disturbed NO-ROS balance in the SHR dam persistently affects BP in her offspring. Dietary supplements, which support NO formation and scavenge ROS, administered during pregnancy and lactation resulted in persistently lower BP for up to 48 wk in SHR offspring. The NO donor molsidomine and the superoxide dismutase mimic tempol-induced comparable effects. Specific inhibition of inducible nitric oxide synthase (NOS) reduces BP in adult SHR, suggesting that inducible NOS is predominantly a source of ROS in SHR. Indeed, inducible NOS inhibition in SHR dams persistently reduced BP in adult offspring. Persistent reductions in BP were accompanied by prevention of proteinuria in aged SHR. We propose that in SHR the known increase in ANG II type 1 receptor density during development leads to superoxide production, which enhances inducible NOS activity. The relative shortage of substrate and cofactors leads to uncoupling of inducible NOS, resulting in superoxide production, activating transcription factors that subsequently again increase inducible NOS expression. This vicious circle probably is perpetuated into adult life. spontaneously hypertensive rat; nitric oxide; inducible nitric oxide synthase; molsidomine; tempol; proteinuria THERE IS NOW A LARGE BODY of epidemiological data proving that environmental factors acting early in life, in particular in the intrauterine and postnatal period, correlate with chronic cardiovascular diseases. From these observations, Barker (10) developed the "programming hypothesis," which proposes that fetal adaptation to adverse environmental factors in the perinatal period results in permanent structural and physiological changes that manifest as disease in adult life. As such, fetal programming is a form of phenotypic plasticity (10), which has conveyed an evolutionary advantage in the past but now has adverse effects because of relatively rapid changes in the environment in which we live (58). An example of this may be the explosion of hyperten...

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The effects of anaemia on heart, placenta and body weight, and blood pressure in fetal and neonatal rats.

Cited by 97 publications

References 14 publications

Long-Term Circulatory Consequences of Perinatal Iron Deficiency in Male Wistar Rats

Long-Term Circulatory Consequences of Perinatal Iron Deficiency in Male Wistar Rats

Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon

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