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Cardiac remodeling in chronic hypertension during murine pregnancy

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Chronic hypertension affects 3-5% of pregnancies, presenting a combination of pressure and volume overload with opposing effects on cardiac function [1]. However, the influence of these competing forces on cardiac remodeling in hypertensive pregnancy remains unclear. Using a murine model, we aimed to characterize cardiac remodeling, hypothesizing that pregnancy may counteract hypertension-related declines in cardiac function. Nulliparous female C57Bl6/J mice (10-13 weeks old) were implanted with 42-day mini-osmotic pumps (Azlet Durect) loaded with angiotensin II (1000 ng/kg/min) to induce hypertension. Animals were randomly assigned into hypertensive control (AngII, n=7) and hypertensive pregnancy (AngII+Preg, n=5) groups. We collected tail-cuff blood pressure, and 2D and 4D high-frequency ultrasound (MX550D, 40 MHz center frequency, Vevo3100, VisualSonics) images of the left ventricle at baseline, 14 days after pump implantation, gestational (e) days 6.5, 12.5, 15.5, 18.5, and on postpartum (p) day 1. Statistical significance was assessed by two-way ANOVA ( p <0.05). Ejection fraction was maintained across both animal groups throughout the experimental timeline. Stroke volume (SV), however, decreased in the AngII group and increased in the AngII+Preg group compared to baseline, and by gestational day (e) 15 was significantly higher in the AngII+Preg group (30.4 ± 7.4 uL vs. 21.5± 6.1 uL, AngII+Preg vs. AngII). Similar to SV, cardiac output decreased in the AngII group and increased the AngII+Preg group (12.0 ± 3.6 uL vs. 16.3 ± 4.3 uL, AngII vs AngII+Preg, eday 15). Excised heart mass was greater in the AngII group at 190.7 ± 21.1 mg compared to 158.0 ± 10.7mg in the AngII+Preg group on pday 1. These results suggest that adaptations during pregnancy may alter cardiac remodeling in the settings of hypertension. Ongoing histology and 4D strain mapping may be helpful to further identify related changes in tissue geometry and biomechanics. Findings from this work could provide insight into the pathophysiology of chronic hypertension in pregnancy and set the foundation for future efforts in identifying patient risk factors, ultimately improving standard of care for both mother and child. [1] Lawler, et al., Hypertens Pregnancy. 2007. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Title: Cardiac remodeling in chronic hypertension during murine pregnancy
Description:
Chronic hypertension affects 3-5% of pregnancies, presenting a combination of pressure and volume overload with opposing effects on cardiac function [1].
However, the influence of these competing forces on cardiac remodeling in hypertensive pregnancy remains unclear.
Using a murine model, we aimed to characterize cardiac remodeling, hypothesizing that pregnancy may counteract hypertension-related declines in cardiac function.
Nulliparous female C57Bl6/J mice (10-13 weeks old) were implanted with 42-day mini-osmotic pumps (Azlet Durect) loaded with angiotensin II (1000 ng/kg/min) to induce hypertension.
Animals were randomly assigned into hypertensive control (AngII, n=7) and hypertensive pregnancy (AngII+Preg, n=5) groups.
We collected tail-cuff blood pressure, and 2D and 4D high-frequency ultrasound (MX550D, 40 MHz center frequency, Vevo3100, VisualSonics) images of the left ventricle at baseline, 14 days after pump implantation, gestational (e) days 6.
5, 12.
5, 15.
5, 18.
5, and on postpartum (p) day 1.
Statistical significance was assessed by two-way ANOVA ( p <0.
05).
Ejection fraction was maintained across both animal groups throughout the experimental timeline.
Stroke volume (SV), however, decreased in the AngII group and increased in the AngII+Preg group compared to baseline, and by gestational day (e) 15 was significantly higher in the AngII+Preg group (30.
4 ± 7.
4 uL vs.
21.
5± 6.
1 uL, AngII+Preg vs.
AngII).
Similar to SV, cardiac output decreased in the AngII group and increased the AngII+Preg group (12.
0 ± 3.
6 uL vs.
16.
3 ± 4.
3 uL, AngII vs AngII+Preg, eday 15).
Excised heart mass was greater in the AngII group at 190.
7 ± 21.
1 mg compared to 158.
0 ± 10.
7mg in the AngII+Preg group on pday 1.
These results suggest that adaptations during pregnancy may alter cardiac remodeling in the settings of hypertension.
Ongoing histology and 4D strain mapping may be helpful to further identify related changes in tissue geometry and biomechanics.
Findings from this work could provide insight into the pathophysiology of chronic hypertension in pregnancy and set the foundation for future efforts in identifying patient risk factors, ultimately improving standard of care for both mother and child.
[1] Lawler, et al.
, Hypertens Pregnancy.
2007.
This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format.
There is no downloadable file or PDF version.
The Physiology editorial board was not involved in the peer review process.

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