Structure adaptation and blood flow control in the uterine arterial system after hemochorial placentation

Moll, W.

doi:10.1016/s0301-2115(03)00169-6

Cited by 54 publications

(39 citation statements)

References 33 publications

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“…In human and rodent pregnancy, maternal uteroplacental vascular resistance is mainly regulated by the vascular tone of uterine radial arteries. These vessels connect large main and arcuate uterine arteries with spiral arteries; the latter vessels are characterized by their significant enlargement and loss of contractility due to trophoblast invasion (12,52,55). The effect of experimental diabetes on endothelium-mediated vasodilation of uteroplacental radial arteries remains unexplored and was the major objective of the present study.…”

mentioning

confidence: 94%

“…The strongest correlation between abnormal uterine artery Doppler waveform and adverse pregnancy outcome has been reported in diabetic pregnant women with preexisting vascular complications (59). Impaired uteroplacental blood flow was also documented in a rodent model of streptozotocin (STZ)-induced diabetes and a mouse model of gestational diabetes (14,25,63,64).Normal pregnancy is characterized by a marked increase in uterine blood flow due to growth and remodeling of the uterine vasculature as well as enhanced endothelium-dependent uterine vasodilation (8,33,52,55). Therefore, multiple causes might be responsible for the reduced uteroplacental blood flow in diabetic pregnancies, including functional abnormalities in the maternal uteroplacental vasculature.…”

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confidence: 99%

“…Normal pregnancy is characterized by a marked increase in uterine blood flow due to growth and remodeling of the uterine vasculature as well as enhanced endothelium-dependent uterine vasodilation (8,33,52,55). Therefore, multiple causes might be responsible for the reduced uteroplacental blood flow in diabetic pregnancies, including functional abnormalities in the maternal uteroplacental vasculature.…”

mentioning

confidence: 99%

“…Radial arteries are located between the main uterine artery and placenta. Physiological levels of pressure measured in these vessels in vivo are 1/3 to 2/3 of central arterial pressure that approximate 40 -70 mmHg (52).…”

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confidence: 99%

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Role of impaired endothelial cell Ca²⁺signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Gokina

Bonev

Gokin

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Gokina NI, Bonev AD, Gokin AP, Goloman G. Role of impaired endothelial cell Ca 2ϩ signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy. Am J Physiol Heart Circ Physiol 304: H935-H945, 2013. First published February 1, 2013 doi:10.1152/ajpheart.00513.2012.-Diabetes mellitus in pregnancy is associated with impaired endothelium-mediated dilatation of maternal arteries, although the underlying cellular mechanisms remain unknown. In this study, we hypothesized that diabetes during rat gestation attenuates agonist-induced uterine vasodilation through reduced endothelial cell (EC) Ca 2ϩ elevations and impaired smooth muscle cell (SMC) hyperpolarization and SMC intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) responses. Diabetes was induced by an injection of streptozotocin to second-day pregnant rats and confirmed by the development of maternal hyperglycemia. Control rats were injected with a citrate buffer. Fura-2-based measurements of SMC [Ca 2ϩ ]i or microelectrode recordings of SMC membrane potential were performed concurrently with dilator responses to ACh in uteroplacental arteries from control and diabetic pregnant rats. ]i elevations were significantly reduced by diabetes. In conclusion, these data demonstrate that reduced endothelium-mediated hyperpolarization contributes to attenuated uteroplacental vasodilation and SMC [Ca 2ϩ ]i responses to ACh in diabetic pregnancy. Impaired endothelial Ca 2ϩ signaling is in part responsible for endothelial dysfunction in the uterine resistance vasculature of diabetic rats. Pharmacological improvement of EC Ca 2ϩ handling may provide an important strategy for the restoration of endothelial function and enhancement of maternal blood flow in human pregnancies complicated by diabetes. endothelial dysfunction; acetylcholine-induced hyperpolarization; fura-2; calcium signaling; pressurized arteries DIABETES MELLITUS is one of the most common medical complications of pregnancy that significantly contributes to maternal and perinatal morbidity and mortality (5,7,11,13,44). The worldwide rise in obesity among women of childbearing age is in part responsible for the increased prevalence of diabetes during pregnancy (44, 47). Pregestational and gestational diabetes are serious complications with short-and long-term consequences for both offspring and mothers. Despite the improvement in perinatal outcome in well-controlled diabetic pregnancies, problems related to abnormal fetal growth, stillbirth, and congenital malformations persist (13). Women with gestational and especially pregestational diabetes are also at higher risk for the development of hypertension and preeclampsia during pregnancy (5,10,60,61,68).Human diabetic pregnancy is associated with an increased vascular resistance in the maternal uteroplacental circulation. The prevalence of an abnormal uterine artery Doppler velocity waveform is much higher in diabetic than nondiabetic populations (6, 9, 39, 59). The strongest correlation between abnormal uterine artery Doppler waveform and adverse ...

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confidence: 94%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Role of impaired endothelial cell Ca²⁺signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Gokina

Bonev

Gokin

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…The uterine vessels undergo marked elongation during uterine growth that is a unique structural change in the uterine vasculature. [5][6][7] The circumferential vascular remodeling associated with normal pregnancy has been characterized as outward hypertrophic, with increases in both lumen diameter and cross-sectional area via smooth muscle cell hypertrophy and hyperplasia. 5,8,9 This phenomenon has been shown in both the main uterine artery (MUA) as well as in the smaller uterine resistance arteries in multiple species including sheep, pigs, rats, and humans.…”

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confidence: 99%

Impact of Experimental Diabetes on the Maternal Uterine Vascular Remodeling During Rat Pregnancy

et al. 2012

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Normal pregnancy is associated with an increase in uteroplacental blood flow in part due to growth and remodeling of the maternal uterine vasculature. In this study, we characterized the effect of diabetic pregnancy on vascular growth of the maternal uterine vasculature and on the passive mechanical properties of the uterine resistance arteries. Diabetes was induced in pregnant rats by injection of streptozotocin and confirmed by development of hyperglycemia. Fetuses of diabetic rats were significantly smaller and placentas larger compared to controls. Pregnancy-induced axial elongation of the mesometrial uterine vasculature was not altered by diabetes. Vascular wall thickness was unchanged between groups. Wall distensibility was increased and the rate constant of an exponential function fitted to stress-strain curve was significantly reduced demonstrating decreased wall stiffness in diabetic uterine radial arteries compared to controls. We conclude that experimental diabetes in rat pregnancy does not compromise the growth of maternal uterine vasculature but alters passive mechanical properties of the uterine radial arteries.

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Separation and characterization of maternal cardiac and vascular sounds in the third trimester of pregnancy

Riknagel

Zimmermann²,

Farlie

et al. 2017

Intl J Gynecology & Obste

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Structure adaptation and blood flow control in the uterine arterial system after hemochorial placentation

Cited by 54 publications

References 33 publications

Role of impaired endothelial cell Ca²⁺signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Role of impaired endothelial cell Ca²⁺signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Impact of Experimental Diabetes on the Maternal Uterine Vascular Remodeling During Rat Pregnancy

Separation and characterization of maternal cardiac and vascular sounds in the third trimester of pregnancy

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Structure adaptation and blood flow control in the uterine arterial system after hemochorial placentation

Cited by 54 publications

References 33 publications

Role of impaired endothelial cell Ca2+signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Role of impaired endothelial cell Ca2+signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Impact of Experimental Diabetes on the Maternal Uterine Vascular Remodeling During Rat Pregnancy

Separation and characterization of maternal cardiac and vascular sounds in the third trimester of pregnancy

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Role of impaired endothelial cell Ca²⁺signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Role of impaired endothelial cell Ca²⁺signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy