Placental expression of the angiogenic placental growth factor is stimulated by both aldosterone and simulated starvation

Eisele, Nicole; Albrecht, Christiane; Mistry, Hiten D.; Dick, Bernhard; Baumann, Marc; Surbek, Daniel; Currie, Gemma; Delles, Christian; Mohaupt, Markus; Escher, Geneviève; Gennari-Moser, Carine

doi:10.1016/j.placenta.2016.02.004

Cited by 16 publications

(8 citation statements)

References 29 publications

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“…Lower PlGF concentrations in women with both PE and SPE compared with those with CKD without SPE and NCs is consistent with our previous findings [22] and further highlights this as a useful diagnostic tool for both PE and SPE. The similar pattern of changes seen for PlGF with renin and aldosterone strengthens previously identified associations of PlGF and RAAS activation [24, 45]. Further work to fully elucidate mechanisms of regulation between angiogenic imbalance and the RAAS in early pregnancy is required.…”

Section: Discussionsupporting

confidence: 81%

“…Urinary TH-aldo concentrations are also relatively lower in pregnancies complicated by PE compared with NCs and are likely to contribute to decreased volume expansion and subsequent poor placental perfusion. We have previously reported urinary TH-aldo levels to be correlated with placental weight and proliferation of cultured trophoblasts is increased upon aldosterone stimulation [24]. Our finding that urinary TH-aldo: creatinine ratios are also lower in SPE compared with women with CKD who did not develop SPE further suggests that this finding is a PE-specific alteration.…”

Section: Discussionsupporting

confidence: 50%

“…Recently, we have shown that PlGF could be used as a potential marker to assist clinical decision-making in women with SPE [22]. We and others have also previously reported PlGF associations with the components of the RAAS [23, 24]; in particular, aldosterone can stimulate PlGF in placental (BeWo) and adrenocortical (H295R) cell lines [24].…”

Section: Introductionmentioning

confidence: 98%

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Responses of the renin–angiotensin–aldosterone system in pregnant chronic kidney disease patients with and without superimposed pre-eclampsia

Kurlak

Pipkin

Mohaupt

et al. 2019

Clinical Kidney Journal

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BackgroundWomen with chronic kidney disease (CKD) are at increased risk of superimposed pre-eclampsia (SPE). Accurate identification of SPE is challenging. We hypothesized that specific components of the renin–angiotensin–aldosterone system (RAAS) would discriminate between CKD and SPE. The aim of the study was to establish differences in circulating and intrarenal RAAS in women with CKD with and without SPE and compare these to normotensive controls (NCs) and women with pre-eclampsia (PE).MethodsWhite European NC women (n = 20), women with PE (n = 9), normotensive CKD without SPE (n = 8) and with SPE (n = 11) were recruited in the third trimester. Plasma renin, plasma and urine total angiotensinogen (AGT) concentrations were quantified by enzyme-linked immunosorbent assay, urinary tetrahydroaldosterone (TH-aldo) concentration by gas chromatography-mass spectrometry and placental growth factor (PlGF) by immunoassay.ResultsUrinary TH-aldo:creatinine ratios were lower in women with PE or SPE compared with NC or women with CKD (P < 0.05 for all). The same group differences were observed for plasma active renin and PlGF concentrations (P < 0.05 for all). Urine total AGT was higher in women with PE compared with NC (P < 0.05) and urine TH-aldo:urine AGT was lower (P < 0.05). However, women with SPE had lower urinary AGT concentrations compared with women with PE (P < 0.05). No differences in plasma total AGT were observed between groups.ConclusionsWomen with SPE have a lower urinary TH-aldo:creatinine ratio, lower plasma active renin and lower PlGF concentrations than women with CKD, comparable to women with PE without pre-existing disease, suggestive of similar pathophysiology. These data suggest disruption of the RAAS pathway in SPE similar to PE. Exploration of the predictive value of RAAS components for adverse pregnancy events in women with CKD is required.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 50%

Section: Introductionmentioning

confidence: 98%

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Responses of the renin–angiotensin–aldosterone system in pregnant chronic kidney disease patients with and without superimposed pre-eclampsia

Kurlak

Pipkin

Mohaupt

et al. 2019

Clinical Kidney Journal

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“…In pregnancy, aldosterone levels are high despite plasma volume expansion and also less responsive to increased Na + intake. This volume expansion does not translate into the expected rise in blood pressure (BP),5 only partially explained by the aldosterone‐induced release of vasodilatory placental growth factor 6…”

Section: Introductionmentioning

confidence: 99%

Physiological and Molecular Responses to Altered Sodium Intake in Rat Pregnancy

Eisele

Klossner

Escher

et al. 2018

JAHA

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BackgroundIn pregnancy, a high plasma volume maintains uteroplacental perfusion and prevents placental ischemia, a condition linked to elevated maternal blood pressure (BP). Reducing BP by increasing Na+ intake via plasma volume expansion appears contra‐intuitive. We hypothesize that an appropriate Na+ intake in pregnancy reduces maternal BP and adapts the renin‐angiotensin system in a pregnancy‐specific manner.Methods and Results BP was measured by implanted telemetry in Sprague‐Dawley rats before and throughout pregnancy. Pregnant and nonpregnant animals received either a normal‐salt (0.4%; NS), high‐salt (8%; HS), or low‐salt (0.01%; LS) diet, or HS (days 1–14) followed by LS (days 14–20) diet (HS/LS). Before delivery (day 20), animals were euthanized and organs collected. Food, water, and Na+ intake were monitored in metabolic cages, and urinary creatinine and Na+ were analyzed. Na+ intake and retention increased in pregnancy (NS, LS), leading to a positive Na+ balance (NS, LS). BP was stable during LS, but reduced in HS conditions in pregnancy. The renin‐angiotensin system was adapted as expected. Activating cleavage of α‐ and γ‐subunits of the renal epithelial Na+ channel and expression of‐full length medullary β‐subunits, accentuated further in all LS conditions, were upregulated in pregnancy.ConclusionsPregnancy led to Na+ retention adapted to dietary changes. HS exposure paradoxically reduced BP. Na+ uptake while only modestly linked to the renin‐angiotensin system is enhanced in the presence of posttranslational renal epithelial Na+ channel modifications. This suggests (1) storage of Na+ in pregnancy upon HS exposure, bridging periods of LS availability; and (2) that potentially non–renin‐angiotensin–related mechanisms participate in ENaC activation and consecutive Na+ retention.

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“…Recently, extrarenal aldosterone effect in pregnancy has been reported. It is an important factor supporting normal placental development and trophoblast cell proliferation via placental growth factor (PLGF) stimulation [12]. In physiological pregnancy aldosterone/renin ratio increases which suggests an influence of additional factors on elevated aldosterone synthesis, other than those within the RAAS.…”

mentioning

confidence: 99%

Renin-Angiotensin-Aldosterone System in the Pathogenesis of Pregnancy-Induced Hypertension

Świątkowska−Stodulska

Kmieć

Stefańska

et al. 2018

Exp Clin Endocrinol Diabetes

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Hypertension occurs in 7-10% of pregnant women. Despite the continuous development of medicine, it is still an important risk factor for perinatal mortality of both mothers and fetuses. Pregnant women with hypertension are at greater risk of complications such as: placental abruption, cerebral and cardiac incidents, multiorgan failure, and disseminated intravascular coagulation. The aim of this review was to discuss multilevel disorders of the renin-angiotensin-aldosterone system in the etiopathogenesis of pregnancy-induced hypertension.

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Placental expression of the angiogenic placental growth factor is stimulated by both aldosterone and simulated starvation

Cited by 16 publications

References 29 publications

Responses of the renin–angiotensin–aldosterone system in pregnant chronic kidney disease patients with and without superimposed pre-eclampsia

Responses of the renin–angiotensin–aldosterone system in pregnant chronic kidney disease patients with and without superimposed pre-eclampsia

Physiological and Molecular Responses to Altered Sodium Intake in Rat Pregnancy

Renin-Angiotensin-Aldosterone System in the Pathogenesis of Pregnancy-Induced Hypertension

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