Impact of gestational stress on postpartum endothelial function

Q: What is the clinical evidence from this study?

Population: Postpartum endothelial dysfunction induced by gestational stress. Intervention: Variable stress (VS) protocol (isolation, wet sawdust, cage tilt, food/water deprivation) vs. Unstressed control group. Primary outcome: Maximum endothelium-dependent relaxation of thoracic aorta induced by acetylcholine at 21 days postpartum (MD -25.21%, p=0.048).

Q: What does this research mean for the field?

Variable stress during late gestation causes persistent postpartum endothelial dysfunction characterized by impaired acetylcholine-induced aortic relaxation, increased phenylephrine sensitivity, and decreased phosphorylated eNOS expression in rats. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Pedro Ribeiro de Souza; Juliana Arruda de Souza Monnerat; Bianca Bittencourt Lucchetti; Juliana Mentzinger; Gabriel Fernandes Teixeira; Natália G. Rocha; Fernanda Brito; Gabriel Ferreira Lima; Nadia Alice Vieira Motta; Anna Caldas Manhães; Vinicius Nogueira Macedo; Natalia Galito Rocha; Antonio Cláudio Lucas da Nóbrega; Renata Frauches Medeiros

doi:10.14814/phy2.71171

November 1, 2026Physiological ReportsOpen Access

Impact of gestational stress on postpartum endothelial function

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Key result

Gestational stress reduces postpartum maximal aortic relaxation by ~25 percentage points via lower eNOS expression.

MD -25.21%
P=0.048

Figures

Graphical abstract published by Physiological Reports — Graphical abstract · Published by Physiological Reports · CC BY

Why the study?

Variable stress is associated with increased cardiovascular risk that may be intensified during pregnancy, but its cardiovascular impacts on maternal health are not yet understood.

Does variable stress during the third week of gestation impair postpartum endothelial function and vascular reactivity in female Wistar rats?

Key Points

To evaluate the impact of variable stress during pregnancy on maternal endothelial function and vascular reactivity in Wistar rats during the postpartum period.
Pregnant 90-day-old Wistar rats were divided into a control group and a variable stress group subjected to daily unpredictable stressors from gestational days 14 to 21.
Following a 21-day lactation period, dams were euthanized, and blood and thoracic aorta were collected for vascular reactivity assays, platelet aggregometry, and western blotting.
Dams exposed to variable stress exhibited significantly higher corticosterone levels (p = 0.04) and increased ADP-induced platelet aggregation (p = 0.02) compared to controls.
Aortic rings from stressed dams showed greater sensitivity to phenylephrine (p = 0.05), reduced acetylcholine-mediated relaxation (p = 0.048), and lower expression of eNOSp ser1177 (p = 0.007).

Structured PICO

Does variable stress during the third week of gestation impair postpartum endothelial function and vascular reactivity in female Wistar rats?

P

Population

90-day-old pregnant female Wistar rats subjected to an 8-day variable stress protocol during the third week of gestation and followed for 21 days postpartum until the end of lactation.

I

Intervention

Variable stress (VS) protocol applied daily for 8 days during the third week of gestation (14th to 21st gestational day), consisting of 4 non-consecutive stimuli performed twice each: isolation for 60 min (days 1 and 5), wet sawdust for 24 h (days 2 and 6), cage tilt of 5 cm for 24 h (days 3 and 7), and food/water deprivation for 6 h from 3 pm to 9 pm (days 4 and 8). Both groups received standard commercial rodent food and water ad libitum.

C

Comparator

Control pregnant female Wistar rats not subjected to the variable stress protocol, housed individually with standard commercial rodent food and water ad libitum.

O

Outcome

Postpartum endothelial function and vascular reactivity of thoracic aortic rings (sensitivity to phenylephrine and acetylcholine-induced endothelium-dependent relaxation) measured after the 21-day lactation period.surrogate

Main Result

Mean Difference: -25.21

Absolute Event Rate: 78.79% vs 104%

p-value: p=0.048

In a preclinical rat model, exposure to variable stress during late gestation caused persistent postpartum maternal endothelial dysfunction, vascular hyperreactivity, reduced eNOS activation, and increased platelet aggregation that persisted even after lactation.

Limitations

Preclinical animal model (Wistar rats)
Pharmacological inhibition of NOS was not performed, limiting direct demonstration of the role of nitric oxide in the observed vascular effects
Sample size per group is not explicitly stated in the methods
Pharmacological inhibition of nitric oxide synthase (NOS) was not performed, which limits the direct demonstration of the role of nitric oxide in the observed vascular effects.

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Implication

Suggests persistent postpartum endothelial dysfunction after gestational stress in rats; hypothesis-generating and should not change clinical practice.

Abstract

Variable stress (VS) is associated with increased cardiovascular risk, and its effects may be intensified during pregnancy. However, the cardiovascular impacts of VS during pregnancy on maternal health are not yet understood. Thus, the aim of this study was to evaluate the impact of VS during gestation on the endothelial function of Wistar rats in the postpartum period. Pregnant rats were divided into Control (C) and VS groups. Stress protocol was applied during the third week of gestation and lasted 8 days. After the lactation period, thoracic aorta and blood were collected for vascular reactivity assessment and platelet aggregation evaluation. Protein abundance was evaluated by western blot. Mothers who experienced VS had higher levels of corticosterone ( p = 0.04), confirming the effectiveness of the model. VS animals showed greater sensitivity ( p = 0.05) to phenylephrine and reduced relaxation by acetylcholine ( p = 0.048), as well as a lower expression of eNOSp ser1177 ( p = 0.007) and increased platelet aggregation ( p = 0.02). Variable stress at the end of gestation seems to cause alterations in both the vasoconstrictor response and endothelium‐dependent vasodilation and may be related to reduced eNOS activation that persists even after lactation.

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Cite This Study

Souza et al. (2026) studied Postpartum endothelial dysfunction induced by gestational stress. Variable stress (VS) protocol (isolation, wet sawdust, cage tilt, food/water deprivation) vs. Unstressed control group was evaluated on Maximum endothelium-dependent relaxation of thoracic aorta induced by acetylcholine at 21 days postpartum (MD -25.21%, p=0.048). Gestational variable stress reduced postpartum acetylcholine-induced maximal aortic relaxation by 25.21% and lowered phosphorylated eNOS expression in rats.

synapsesocial.com/papers/6af5cd33a40bbe8669e89cab https://doi.org/10.14814/phy2.71171

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Impact of gestational stress on postpartum endothelial function

Figures

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Impact of gestational stress on postpartum endothelial function

Figures

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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