Mechanisms of endothelium-dependent vasodilation in male and female, young and aged offspring born growth restricted

Morton, Jude S.; Rueda-Clausen, Christian F.; Davidge, Sandra T.

doi:10.1152/ajpregu.00641.2009

Cited by 77 publications

(107 citation statements)

References 41 publications

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“…For example, prenatal hypoxia has been shown to reduce NO dependence in vascular tone and promote endothelial-derived hyperpolarization-mediated vasodilation. 20 Whether this shift in vascular control mechanisms by Resv supplementation during development is mediated by hypoxia-related signaling is an intriguing hypothesis, particularly because Resv is known to interfere with hypoxiainducible factor expression and adaptations to hypoxia. 21 In addition to contributing to resting vascular tone, NO has myriad functions, including physiological antagonism of vasoactive mediators, such as ET-1.…”

Section: Discussionmentioning

confidence: 99%

“…11 We have previously shown that NO modulates cleavage of bET-1 to active ET-1, 22 and this pathway is perturbed in offspring that exhibit a reduced NO-mediated vasodilation. 20,23 We therefore investigated the role of bET-1 conversion to active ET-1 in baseline and l-NAME-induced hypertension in adult offspring. The endothelin-converting enzyme inhibitor CGS attenuated the l-NAME-induced rise in BP, without affecting baseline BP, thus confirming our previous reports that NO tonically inhibits the actions of ET-1, in part by inhibiting the conversion of bET-1 to active ET-1.…”

Section: Discussionmentioning

confidence: 99%

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Perinatal Resveratrol Supplementation to Spontaneously Hypertensive Rat Dams Mitigates the Development of Hypertension in Adult Offspring

et al. 2016

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ypertension is an important and modifiable risk factor for cardiovascular disease, affecting ≈1 in 4 adults worldwide. 1 In the United States, hypertension is estimated to account for >$46 billion annually in healthcare services, medication, and lost productivity, 2 and these costs are expected to increase substantially over the coming decades. A universal consensus is that prevention, rather than treatment, is a more strategic and cost-effective approach to reducing the burden of cardiovascular disease in coming decades.Essential hypertension, in which known primary causes (eg, renovascular disease, pheochromocytoma, monogenic causes, etc) are not present, makes up 95% of hypertension worldwide.3 Although the pathogenesis of essential hypertension is multifactorial and complex, subclinical changes in vascular function often precede the development of hypertension and circulatory decline. 4 The spontaneously hypertensive rat (SHR) is a model of essential hypertension in which blood pressure (BP) begins to rise after 6 weeks of age, ultimately reaching stable pressures of ≈180 to 200 mm Hg. Recently, Komolova et al reported evidence of altered vascular resistance profiles and renal hemodynamics as early as 3 weeks of age in the SHR, 5 implicating these early functional changes as a cause, rather than a consequence, of hypertension in this model. As such, the developmental period before weaning (ie, See Editorial Commentary, pp 829-830Abstract-This study was undertaken to determine whether perinatal maternal resveratrol (Resv)-a phytoalexin known to confer cardiovascular protection-could prevent the development of hypertension and improve vascular function in adult spontaneously hypertensive rat offspring. Dams were fed either a control or Resv-supplemented diet (4 g/kg diet) from gestational day 0.5 until postnatal day 21. Indwelling catheters were used to assess blood pressure and vascular function in vivo; wire myography was used to assess vascular reactivity ex vivo. Perinatal Resv supplementation in dams had no effect on fetal body weights, albeit continued maternal treatment postnatally resulted in growth restriction in offspring by postnatal day 21; growth restriction was no longer evident after 5 weeks of age. Maternal perinatal Resv supplementation prevented the onset of hypertension in adult offspring (−18 mm Hg; P=0.007), and nitric oxide synthase inhibition (with l-NG-nitroarginine methyl ester) normalized these blood pressure differences, suggesting improved nitric oxide bioavailability underlies the hemodynamic alterations in the Resv-treated offspring. In vivo and ex vivo, vascular responses to methylcholine were not different between treatment groups, but prior treatment with l-NG-nitroarginine methyl ester attenuated the vasodilation in untreated, but not Resv-treated adult offspring, suggesting a shift toward nitric oxide-independent vascular control mechanisms in the treated group. Finally, bioconversion of the inactive precursor big endothelin-1 to active endothelin-1 in isolated mesenteric art...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Perinatal Resveratrol Supplementation to Spontaneously Hypertensive Rat Dams Mitigates the Development of Hypertension in Adult Offspring

et al. 2016

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“…[21][22][23] Studies such as these have reported that chronic fetal hypoxia can program persistent pulmonary hypertension in the newborn and pulmonary hypertension in the adult offspring. 24 However, because maternal exposure to hypoxia can lead to a significant decrease in maternal food intake, 25 the extent to which any adverse effects on the pulmonary circulation of the offspring are due to under-nutrition and/or under-oxygenation, once again, remain unclear.…”

mentioning

confidence: 99%

High-Altitude Hypoxia and Echocardiographic Indices of Pulmonary Hypertension in Male and Female Chickens at Adulthood

Salinas

Blanco

Villena

et al. 2014

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ditions, again, remain uncertain.Experimental studies in animal models, including our own, have used exposure of pregnant mammals to chronic hypobaric or isobaric hypoxia during gestation and have studied the effects on fetal growth and on the cardiovascular system of the offspring in the newborn and adult periods. 21-23 Studies such as these have reported that chronic fetal hypoxia can program persistent pulmonary hypertension in the newborn and pulmonary hypertension in the adult offspring. 24 However, because maternal exposure to hypoxia can lead to a significant decrease in maternal food intake, 25 the extent to which any adverse effects on the pulmonary circulation of the offspring are due to under-nutrition and/or under-oxygenation, once again, remain unclear.The combination of HA exposure with the use of the chick embryo model permits investigation of the direct effects of HA hypoxia on growth and on cardiovascular development completely independent of alterations in placental function, independent of changes in the maternal physiology and independent of any effects of socioeconomic factors. Previously, we ulmonary hypertension continues to be an important clinical problem. 1-8 Studies of populations at high altitude (HA) have unequivocally reported intrauterine growth restriction (IUGR) and a higher prevalence of pulmonary hypertension, 9-17 suggesting that a component of these conditions is associated with exposure to chronic hypoxia. However, because most highland populations are also impoverished, the relative contributions of chronic hypoxia or of chronic malnutrition during the fetal and postnatal periods in stunting growth and promoting pulmonary vascular disease during life at altitude remain uncertain.Similarly, clinical studies at sea level (SL) have reported an association between the IUGR infant and the early development of right ventricular dysfunction and pulmonary hypertension. 18-20 However, because IUGR in human high-risk pregnancy normally occurs as a result of increased placental vascular impedance with consequent falls in oxygen and nutrient delivery to the baby, the relative contributions of chronic hypoxia or of chronic malnutrition during the fetal period in slowing growth and promoting pulmonary vascular anomalies under these con- Background: By combining the chick embryo model with incubation at high altitude (HA), the effects of chronic hypoxia on fetal growth, fetal cardiac and aortic wall remodeling and systemic arterial blood pressure at adulthood were reported. Using non-invasive functional echocardiography, here we investigated the in vivo effects of HA hypoxia on the pulmonary circulation at adulthood in male and female chickens.

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“…Пренатальная гипоксия, которая также увеличивает продукцию перекисных агентов, вызывает уменьше-ние у 4-месячных крыс реакции расслабления мезен-териальных сосудов в ответ на действие оксида азота и агентов (метахолина), которые через эндотелий-за-висимые механизмы потенцируют реакции рассла-бления [75]. Интересно, что такой сниженный ответ на оксид азота у нормальных крыс наблюдается толь-ко в пожилом возрасте (18 мес), что подтверждает предположения о том, что оксидативный стресс уско-ряет процессы старения.…”

Section: роль оксидативного стресса как эпигенетического фактораunclassified

Perinatal programming and cardiomyocyte aging

Ковтун¹,

Цывьян²,

Соловьева³

2017

Ross. vestn. perinatol. pediatr.

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Mechanisms of endothelium-dependent vasodilation in male and female, young and aged offspring born growth restricted

Cited by 77 publications

References 41 publications

Perinatal Resveratrol Supplementation to Spontaneously Hypertensive Rat Dams Mitigates the Development of Hypertension in Adult Offspring

Perinatal Resveratrol Supplementation to Spontaneously Hypertensive Rat Dams Mitigates the Development of Hypertension in Adult Offspring

High-Altitude Hypoxia and Echocardiographic Indices of Pulmonary Hypertension in Male and Female Chickens at Adulthood

Perinatal programming and cardiomyocyte aging

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