High-salt diets during pregnancy increases renal vascular reactivity due to altered soluble guanylyl cyclase-related pathways in rat offspring

Lin, Ji; Yin, Xinhua; He, Axin; Bo, Le; Zhou, Xiuwen; Tang, Jiaqi; Gu, Xiuxia; Wu, Jue; Gao, Qinqin; Lv, Jian; Mao, Caiping; Xu, Zhice

doi:10.1016/j.jnutbio.2015.10.009

Cited by 4 publications

(2 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous study pointed that adverse factors during pregnancy could cause poor renal development in offspring. [ 21 ] In this study, prenatal HS decreased the kidney weight in both the fetus and adult offspring, suggesting that high‐sucrose diet during pregnancy has affected kidney development later. However, the lower kidney weight/body‐weight ratio was found in fetus, not in adult offspring, which may be caused by “catch‐up growth” after birth.…”

Section: Discussionmentioning

confidence: 62%

“…[ 20 ] Adverse factors during maternal pregnancy could induce renal reprogramming and vascular dysfunction in the offspring. [ 21 ] However, information on whether and how vascular develops in the interlobar renal arteries of offspring exposed to prenatal high‐sucrose diet is still limited. Thus, present study aims to discuss the effects of maternal high‐sucrose diet during the pregnancy on the function of interlobar renal arteries from the adult offspring.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ‐RXRg‐ROS/Akt Signaling

Feng,

Liu,

Wang

et al. 2024

Molecular Nutrition Food Res

View full text Add to dashboard Cite

ScopePrenatal nutrition imbalance correlates with developmental origin of cardiovascular diseases; however whether maternal high‐sucrose diet (HS) during pregnancy causes vascular damage in renal interlobar arteries (RIA) from offspring still keeps unclear.Methods and resultsPregnant rats are fed with normal drinking water or 20% high‐sucrose solution during the whole gestational period. Swollen mitochondria and distributed myofilaments are observed in vascular smooth muscle cells of RIA exposed to prenatal HS. Maternal HS increases phenylephrine (PE)‐induced vasoconstriction in the RIA from adult offspring. NG‐Nitro‐l‐arginine (L‐Name) causes obvious vascular tension in response to PE in offspring from control group, not in HS. RNA‐Seq of RIA is performed to reveal that the gene retinoid X receptor g (RXRg) is significantly decreased in the HS group, which could affect vascular function via interacting with PPARγ pathway. By preincubation of RIA with apocynin (NADPH inhibitor) or capivasertib (Akt inhibitor), the results indicate that ROS and Akt are the vital important factors to affect the vascular function of RIA exposure to prenatal HS.ConclusionMaternal HS during the pregnancy increases PE‐mediated vasoconstriction of RIA from adult offspring, which is mainly related to the enhanced Akt and ROS regulated by the weakened PPARγ‐RXRg.

show abstract

Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ‐RXRg‐ROS/Akt Signaling

Feng,

Liu,

Wang

et al. 2024

Molecular Nutrition Food Res

View full text Add to dashboard Cite

show abstract

Maternal high salt-diet increases offspring's blood pressure with dysfunction of NO/PKGI signaling pathway in heart tissue

Huang

Ren

et al. 2022

gocm

View full text Add to dashboard Cite

BackgroundHigh salt-diets have become significant threats to human health, resulting in hypertension and cardiovascular diseases. Hypertensive disorders during pregnancy are complicated, since the maternal cardiovascular system undergoes extensive physiological changes during pregnancy. High-salt diets during pregnancy can disturb the intrauterine environment and negatively affect fetal development. Therefore, we explored how high-salt diets during pregnancy could affect the offspring.MethodsRats were divided into three groups and fed with low, normal, and high salt diets. The offspring were separated into three groups after weaning based on dietary salt concentration. The blood pressure and urine protein content of both dams and offspring were measured. To evaluate cardiac function, we used Masson staining and immunodetection to confirm the fibrosis status. Finally, we extracted protein from cardiac tissue to test the expression levels of the Nitric Oxide (NO)/cGMP-dependent protein kinase I (PKGI) pathway and the angiotensin receptor.ResultsHigh-salt diets increased blood pressure, and offspring previously exposed to high-salt environments were predisposed to hypertension. High-salt diets were also found to induce cardiac fibrosis and exacerbate fibrosis in offspring and alter the epithelial-mesenchymal transition (EMT). Under these conditions, the NO/PKGI pathway was activated in cardiac tissue and the type-1angiotensin II receptor (AT1R) was upregulated, though the type-2 angiotensin II receptor (AT2R) had the opposite effect.ConclusionHigh-salt diets induce high blood pressure and increase predisposition to hypertension in offspring. They are accompanied by cardiac fibrosis, which could be caused by the activation of NO/PKGI and upregulation of AT1R.

show abstract

Excessive maternal salt intake gives rise to vasopressin-dependent salt sensitivity of blood pressure in male offspring

Kim

Jung

Lee

et al. 2021

Journal of Molecular and Cellular Cardiology

View full text Add to dashboard Cite

High-salt diets during pregnancy increases renal vascular reactivity due to altered soluble guanylyl cyclase-related pathways in rat offspring

Cited by 4 publications

References 32 publications

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ‐RXRg‐ROS/Akt Signaling

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ‐RXRg‐ROS/Akt Signaling

Maternal high salt-diet increases offspring's blood pressure with dysfunction of NO/PKGI signaling pathway in heart tissue

Excessive maternal salt intake gives rise to vasopressin-dependent salt sensitivity of blood pressure in male offspring

Contact Info

Product

Resources

About