Role of the renin–angiotensin–aldosterone system in the enhancement of salt sensitivity caused by prenatal protein restriction in stroke-prone spontaneously hypertensive rats

Otani, Lila; Sugimoto, Naoya; Kaji, Misa; Murai, Mariko; Chang, Shang‐Jen; Kato, Harubumi; Murakami, Tetsuo

doi:10.1016/j.jnutbio.2011.04.014

Cited by 12 publications

(21 citation statements)

References 49 publications

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“…We conclude from these results, as well as those of our previous study, 6) that protein restriction during pregnancy increased ROS sensitivity and salt sensitivity in SHRSP offspring. An appropriate treatment such as administering an antioxidant may therefore be useful to prevent or treat hypertensive vascular injury in mature offspring exposed to a poor intra-uterine environment.…”

Section: Discussionsupporting

confidence: 88%

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Effects of Oxidative Stress on Vascular Reactivity in the Offspring of Protein-Restricted Stroke-Prone Spontaneously Hypertensive Rats

Takemori

Tahara

Murakami

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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Section: Discussionsupporting

confidence: 88%

“…5) Our results also suggested that an increase in aldosterone production in response to highsalt loading was responsible for the enhanced salt sensitivity in the offspring of the protein-restricted dams. 6) Free radicals and reactive oxygen species (ROS) also contribute to the incidence of lifestyle-related diseases (as reviewed by Willcox et al…”

mentioning

confidence: 99%

Effects of Oxidative Stress on Vascular Reactivity in the Offspring of Protein-Restricted Stroke-Prone Spontaneously Hypertensive Rats

Takemori

Tahara

Murakami

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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“…Such effects may be produced by many aspects of the maternal environment, including a maternal high dietary salt intake [5,6,11,17,35,37,40]. In the present study, we tested the hypothesis that a maternal high salt diet during pregnancy and lactation would lead to alterations in cardiac and/or vascular function in offspring.…”

Section: Discussionmentioning

confidence: 96%

“…Vascular health has been found to have many of its origins early in development [42]. Maternal malnutrition has been observed to not only increase the salt sensitivity of blood pressure of offspring [35], but to also impair their vasodilatory response to NO [5,40]. A high salt intake during pregnancy has also been found to raise offspring BP [6,17] and cause a remodeling of heart and arteries in the offspring independent of postnatal salt intake and the BP of the pregnant dams [10,37].…”

Section: Introductionmentioning

confidence: 99%

A maternal high salt diet disturbs cardiac and vascular function of offspring

et al. 2015

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“…Studies in both humans and animals have shown an association between an adverse environment in utero and programming of salt‐sensitive hypertension . The majority of these studies have been carried out in low birth weight individuals and those with intrauterine growth restriction.…”

Section: Introductionmentioning

confidence: 99%

Increased salt sensitivity in offspring of pregnancies complicated by experimental preeclampsia

Yeung

Sunderland

Lind

et al. 2018

Clin Exp Pharma Physio

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Preeclampsia is a hypertensive disorder of pregnancy known to increase the risk of cardiovascular disease in mothers and offspring. Offspring exposed to a suboptimal intrauterine environment may experience altered fetal programming and subsequent long-term cardiovascular changes. This study investigated changes in the vascular response in offspring from experimental preeclampsia (EPE) induced by uterine artery ligation, in the absence of fetal growth restriction, compared to normal baboon pregnancies (controls), following a high salt diet challenge. After 1 week of standard diet (containing <1% salt), animals were fed a high salt diet (6%) for 2 weeks. Systolic and diastolic blood pressure (SBP, DBP), aldosterone, renin and creatinine clearance were evaluated in EPE (n = 6, 50% male) and control (n = 6, 50% male) offspring. A repeated measures analysis was performed, and P < 0.05 was considered significant. At baseline, there were no differences between the groups in any parameter (EPE, mean age and weight 3.2 ± 1.2 years, 6.8 ± 1.0 kg, respectively; Control, 2.9 ± 0.8 years, 7.1 ± 1.5 kg). After salt loading the EPE group had significantly higher SBP (92 ± 5 mm Hg) compared to the control group (83 ± 4 mm Hg, P = 0.03). Aldosterone concentration was higher in the EPE group despite the same salt excretion and no difference in renal function. Salt sensitivity may differ in offspring from hypertensive pregnancies due to fetal programming. This could have long-term consequences for cardiovascular health of EPE offspring and further research is required to determine the exact pathological mechanisms.

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Role of the renin–angiotensin–aldosterone system in the enhancement of salt sensitivity caused by prenatal protein restriction in stroke-prone spontaneously hypertensive rats

Cited by 12 publications

References 49 publications

Effects of Oxidative Stress on Vascular Reactivity in the Offspring of Protein-Restricted Stroke-Prone Spontaneously Hypertensive Rats

Effects of Oxidative Stress on Vascular Reactivity in the Offspring of Protein-Restricted Stroke-Prone Spontaneously Hypertensive Rats

A maternal high salt diet disturbs cardiac and vascular function of offspring

Increased salt sensitivity in offspring of pregnancies complicated by experimental preeclampsia

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