Low birth weight-associated adult hypertension in the rat

Manning, Jennifer; Vehaskari, V. Matti

doi:10.1007/s004670000560

Cited by 135 publications

(168 citation statements)

References 22 publications

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“…4 Vehaskari et al have also examined components of the RAS in offspring from protein-restricted dams and found that plasma renin activity, although reduced in young rats, was elevated in adult rats after establishment of the hypertension. 32 Thus, results from studies using a low-protein model of IUGR suggest that permanent alterations in both structure and physiology do occur in response to fetal undernutrition. 4 -6,10,32 Furthermore, a pathway for fetal programming in this animal model is suggested involving suppression of the RAS during fetal development leading to structural alterations in the kidney with hypertension, 10 followed by activation of the RAS in the adult animal.…”

Section: Discussionmentioning

confidence: 99%

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

et al. 2005

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Abstract-Low birth weight is a risk factor for the subsequent development of hypertension in humans. We previously reported that reduced uterine perfusion in the pregnant rat results in growth-restricted offspring predisposed to the development of hypertension. The purpose of this study was to determine whether the sympathetic nervous system plays a role in mediating hypertension in this model of low birth weight. Key Words: hypertension, pregnancy Ⅲ rats Ⅲ renal nerves Ⅲ denervation Ⅲ sympathetic nervous system H ypertension is a multifactorial disorder thought to result from both genetic and environmental factor interactions. Recent epidemiological studies 1,2 suggest that a predisposition for development of hypertension may be programmed by factors initiated in utero, 3 an observation supported by many animal studies. 4 -7 Fetal malnutrition limits fetal growth and results in small-for-gestational-age newborns. 8,9 Findings from both epidemiological and animal studies suggest that fetal malnutrition may also program or permanently alter fetal structure and physiology, resulting in an increased risk for development of hypertension and cardiovascular disease. 3,10 -12 However, the mechanisms mediating low birth weight (LBW) and hypertension remain to be elucidated.In humans, few studies have examined the relationship between the sympathetic nervous system (SNS) and LBW, and controversy exists with regards to whether LBW individuals are associated with increases [13][14][15] or decreases in sympathetic activity. 16 Evidence for alterations in the SNS is noted in some animal models of intrauterine growth restriction (IUGR), because plasma levels of circulating catecholamines are increased. [17][18][19][20][21] This observation has been noted in growth-restricted offspring from pregnant rats fed a proteinrestricted diet during gestation, 17 in a naturally occurring model of IUGR using piglets, 18,19 and in a model of IUGR induced by placental insufficiency in the rat 20 and in sheep. 21 Additionally, hypoxia during fetal development leads to increased sympathetic innervation. 22,23 However, no further assessment of the SNS in association with IUGR has been examined.Nutrient and oxygen supply limitations are the components of the intrauterine environment that limit fetal growth and result in small-for-gestational-age newborns. Because IUGR within the Western world is more likely the result of reduced uterine perfusion, 24 we have developed a model of fetal programming induced by placental insufficiency caused by hypoxia and fetal undernutrition. 25 Using this model, we previously reported that reduced uterine perfusion initiated at day 14 of gestation in the rat results in growth-restricted offspring that are hypertensive as early as 4 weeks of age. 25 Furthermore, marked elevations in mean arterial pressure (MAP) remain evident in male growth-restricted offspring at 12 weeks of age. Because increased renal sympathetic nerve activity appears to be a causal mechanism in primary hypertension, 26 we determined the ro...

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Section: Discussionmentioning

confidence: 99%

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

et al. 2005

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“…The body weight of offspring was significantly lower in the IUGR and LA groups compared with that in the CON group (P<0.01), which was accompanied by a higher incidence of low-birth-weight (LBW) offspring rats. LBW was defined as less than the average birth weight of the offspring rats in the CON group minus two standard deviations (18). Table II presents a comparison of the body weight and blood glucose levels in the three groups at postnatal weeks 1, 3 and 8.…”

Section: Iugr Model Establishmentmentioning

confidence: 99%

Effect of L-arginine supplementation on the hepatic phosphatidylinositol 3-kinase signaling pathway and gluconeogenic enzymes in early intrauterine growth-restricted rats

Luo

Chen

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate the response of the phosphatidylinositol 3-kinase (PI3K) signaling pathway and gluconeogenic enzymes in intrauterine growth-restricted rats to dietary L-arginine (L-Arg) supplementation during the lactation period early in life. Pregnant Sprague-Dawley rats were randomly divided into a control group (CON), an intrauterine growth restriction group (IUGR) and an L-Arg group (LA). The pregnant rats in the CON group were fed a 21% protein diet, and those in the IUGR and LA groups were fed a 10% low protein diet, and all rats were fed a 21% protein diet after delivery. Water was available ad libitum to the pregnant rats during the 21-day lactation period, and the water provided to the LA group included 200 mg/kg/day L-Arg. Blood glucose, serum insulin, homeostasis model of assessment for insulin resistance (HOMA-IR), PI3K and protein kinase B (PKB) protein expression, and phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase) mRNA expression in the offspring rats were measured postnatally at 1, 3 and 8 weeks. No significant difference in blood glucose, serum insulin and HOMA-IR were identified at any time point among the three groups. PI3K and PKB expression was lower in the IUGR group offspring compared with that in the CON group offspring, but both were increased by dietary L-Arg supplementation. PEPCK mRNA and G-6-Pase mRNA expression levels in the offspring of the IUGR group were higher compared with those in the CON group but were downregulated following L-Arg supplementation. These results suggest that dietary L-Arg supplementation during the early lactation period promoted catch-up growth and reversed abnormalities in hepatic insulin signaling and gene expression of gluconeogenic enzymes in IUGR offspring rats.

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“…Temporal alterations in the RAS are also observed in models of fetal programming (58,60). Plasma renin activity (PRA) remains significantly reduced in young rats from protein restricted dams prior to the development of hypertension (58).…”

Section: The Renin Angiotensin Systemmentioning

confidence: 99%

Section: The Renin Angiotensin Systemmentioning

confidence: 99%

“…Plasma renin activity (PRA) remains significantly reduced in young rats from protein restricted dams prior to the development of hypertension (58). However, PRA becomes significantly increased after the establishment of hypertension (58). ACE inhibition abolishes hypertension in young (59) and adult (58) offspring of protein restricted dams suggesting that RAS played a critical role in the etiology of hypertension programmed by undernutrition in utero.…”

Section: The Renin Angiotensin Systemmentioning

confidence: 99%

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