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

Maruyama, Kana; Kagota, Satomi; Vliet, Bruce N. Van; Wakuda, Hirokazu; Shinozuka, Kazumasa

doi:10.1016/j.lfs.2015.06.023

Cited by 18 publications

(15 citation statements)

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“…In the present study, maternal HSD resulted in changes in the ultrastructure of CAs of 5‐month‐old male offspring, such as myofilament derangements and myofilament breakages. These changes were consistent with previous report that maternal HSD can lead to vascular remodeling, and may thereby lead to changes in vascular functions . We also found that the dense patch's electron density was lowered in HSD group, in comparison to NSD group.…”

Section: Discussionsupporting

confidence: 93%

Maternal high‐salt diet altered PKC/MLC20 pathway and increased ANG II receptor‐mediated vasoconstriction in adult male rat offspring

et al. 2016

Molecular Nutrition Food Res

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Section: Discussionsupporting

confidence: 93%

Maternal high‐salt diet altered PKC/MLC20 pathway and increased ANG II receptor‐mediated vasoconstriction in adult male rat offspring

et al. 2016

Molecular Nutrition Food Res

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“…Maternal high-salt diet during pregnancy may cause cardiac dysfunction in offspring of spontaneously hypertensive rats [2]. Excessive salt intake during pregnancy and lactation is also associated with proteinuria and a low glomerular filtration rate in ninety-day-old Wistar rats [3].…”

Section: Introductionmentioning

confidence: 99%

High and Low Salt Intake during Pregnancy: Impact on Cardiac and Renal Structure in Newborns

et al. 2016

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IntroductionPrevious studies from our laboratory demonstrated that dietary salt overload and salt restriction during pregnancy were associated with cardiac and renal structural and/or functional alterations in adult offspring. The present study evaluated renal and cardiac structure and the local renin-angiotensin system in newborns from dams fed high-, normal- or low-salt diets during pregnancy.MethodsFemale Wistar rats were fed low- (LS, 0.15% NaCl), normal- (NS, 1.3% NaCl) or high- (HS, 8% NaCl) salt diets during pregnancy. Kidneys and hearts were collected from newborns (n = 6-8/group) during the first 24 hours after birth to evaluate possible changes in structure using stereology. Protein expression of renin-angiotensin system components was evaluated using an indirect enzyme-linked immunosorbent assay (ELISA).ResultsNo differences between groups were observed in total renal volume, volume of renal compartments or number of glomeruli. The transverse diameter of the nuclei of cardiomyocytes was greater in HS than NS males in the left and right ventricles. Protein expression of the AT1 receptor was lower in the kidneys of the LS than in those of the NS and HS males but not females. Protein expression of the AT2 receptor was lower in the kidneys of the LS males and females than in those of the NS males and females.ConclusionHigh salt intake during pregnancy induced left and right ventricular hypertrophy in male newborns. Salt restriction during pregnancy reduced the expression of renal angiotensin II receptors in newborns.

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“…Female offspring have lesser increase in BP and even a decrease in BP in some studies [31]. High-salt diet limited to the gestational period or only during weaning [32] may not be associated with hypertension in male or female adult offspring [33]. However, high-salt diet 30 days after birth (dams fed high-salt diet before weaning) increased the BP of adult male offspring [34].…”

Section: Pathogenesis Of Primary Pediatric Hypertensionmentioning

confidence: 99%

“…Twelve-week-old offspring of Sprague-Dawley dams fed high-salt diet had normal BP but had increased wall thickness of central (aorta, carotid), muscular (mesenteric) and intrapulmonary arteries, regardless of the post-weaning diet [36]. Some offspring of high-salt diet-fed dams had low BP and heart rate, indicative of both left ventricular systolic and diastolic function, and decreased aortic vasodilatory response to nitric oxide [32]. Both high and low maternal salt intakes during pregnancy have been reported to decrease nephron number and increase BP in male offspring [37].…”

Section: Pathogenesis Of Primary Pediatric Hypertensionmentioning

confidence: 99%

Primary Pediatric Hypertension: Current Understanding and Emerging Concepts

et al. 2017

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The rising prevalence of primary pediatric hypertension and its tracking into adult hypertension point to the importance of determining its pathogenesis to gain insights into its current and emerging management. Considering that the intricate control of BP is governed by a myriad of anatomical, molecular biological, biochemical, and physiological systems, multiple genes are likely to influence an individual's BP and susceptibility to develop hypertension. The long-term regulation of BP rests on renal and non-renal mechanisms. One renal mechanism relates to sodium transport. The impaired renal sodium handling in primary hypertension and salt sensitivity may be caused by aberrant counter-regulatory natriuretic and anti-natriuretic pathways. The sympathetic nervous and renin-angiotensin-aldosterone systems are examples of antinatriuretic pathways. An important counter-regulatory natriuretic pathway is afforded by the renal autocrine/paracrine dopamine system, aberrations of which are involved in the pathogenesis of hypertension, including that associated with obesity. We present updates on the complex interactions of these two systems with dietary salt intake in relation to obesity, insulin resistance, inflammation, and oxidative stress. We review how insults during pregnancy such as maternal and paternal malnutrition, glucocorticoid exposure, infection, placental insufficiency, and treatments during the neonatal period have long-lasting effects in the regulation of renal function and BP. Moreover, these effects have sex differences. There is a need for early diagnosis, frequent monitoring, and timely management due to increasing evidence of premature target organ damage. Large controlled studies are needed to evaluate the long-term consequences of the treatment of elevated BP during childhood, especially to establish the validity of the current definition and treatment of pediatric hypertension.

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

Cited by 18 publications

References 47 publications

Maternal high‐salt diet altered PKC/MLC20 pathway and increased ANG II receptor‐mediated vasoconstriction in adult male rat offspring

Maternal high‐salt diet altered PKC/MLC20 pathway and increased ANG II receptor‐mediated vasoconstriction in adult male rat offspring

High and Low Salt Intake during Pregnancy: Impact on Cardiac and Renal Structure in Newborns

Primary Pediatric Hypertension: Current Understanding and Emerging Concepts

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