scholarly journals Influence of Estrogens on Uterine Vascular Adaptation in Normal and Preeclamptic Pregnancies

2020 ◽  
Vol 21 (7) ◽  
pp. 2592 ◽  
Author(s):  
Maurizio Mandalà
Keyword(s):  
Heart Rate ◽  
Vascular Remodeling ◽  
Uterine Artery ◽  
Molecular Mechanisms ◽  
Artery Wall ◽  
Successful Pregnancy ◽  
Uteroplacental Blood Flow ◽  
Pathological Pregnancy ◽  
Estrogenic Regulation ◽  
Circulating Levels

During pregnancy, the maternal cardiovascular system undergoes significant changes, including increased heart rate, cardiac output, plasma volume, and uteroplacental blood flow (UPBF) that are required for a successful pregnancy outcome. The increased UPBF is secondary to profound circumferential growth that extends from the downstream small spiral arteries to the upstream conduit main uterine artery. Although some of the mechanisms underlying uterine vascular remodeling are, in part, known, the factors that drive the remodeling are less clear. That higher circulating levels of estrogens are positively correlated with gestational uterine vascular remodeling suggests their involvement in this process. Estrogens binding to the estrogen receptors expressed in cytotrophoblast cells and in the uterine artery wall stimulate an outward hypertrophic remodeling of uterine vasculature. In preeclampsia, generally lower concentrations of estrogens limit the proper uterine remodeling, thereby reducing UPBF increases and restricting the growth of the fetus. This review aims to report estrogenic regulation of the maternal uterine circulatory adaptation in physiological and pathological pregnancy that favors vasodilation, and to consider the underlying molecular mechanisms by which estrogens regulate uteroplacental hemodynamics.

Influence of sleep and myometrial activity on systemic and uteroplacental hemodynamics in pregnant ewes

1995 ◽  
Vol 268 (4) ◽  
pp. H1734-H1739
Author(s):  
J. E. Fewell
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Uterine Artery ◽  
Systemic Arterial Pressure ◽  
Uterine Horn ◽  
Artery Blood Flow ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Quiet Wakefulness ◽  
Uteroplacental Blood Flow

Little is known about the influence of sleep on systemic and uteroplacental hemodynamics during pregnancy. Experiments were therefore carried out on six chronically instrumented pregnant ewes (125–133 days of gestation) to investigate the influence of sleep on systemic and uteroplacental hemodynamics. Because nonlabor myometrial activity influences uteroplacental hemodynamics, we made measurements during quiet wakefulness, quiet sleep, and active sleep in the presence and absence of myometrial activity. Cardiac output, heart rate, and systemic arterial pressure were decreased in active sleep compared with quiet wakefulness; these variables were not significantly altered by myometrial activity. The interaction between sleep and myometrial activity was such that the lowest values of uteroplacental blood flow, as estimated from middle uterine artery blood flow to the pregnant uterine horn and, hence, uteroplacental oxygen delivery occurred during active sleep in the presence of myometrial activity (i.e., decreased approximately 19% compared with quiet wakefulness and the absence of myometrial activity). Further investigation is required to determine the possible fetal consequences of a reduced uteroplacental perfusion in the presence of myometrial activity during sleep.

scholarly journals Molecular Mechanisms Underlying Remodeling of Ductus Arteriosus: Looking beyond the Prostaglandin Pathway

2021 ◽  
Vol 22 (6) ◽  
pp. 3238
Author(s):  
Ho-Wei Hsu ◽  
Ting-Yi Lin ◽  
Yi-Ching Liu ◽  
Jwu-Lai Yeh ◽  
Jong-Hau Hsu
Keyword(s):  
Adverse Effect ◽  
Clinical Management ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Surgical Intervention ◽  
Ductus Arteriosus ◽  
Clinical Problem ◽  
Cyclooxygenase Inhibitors ◽  
Medical Patients ◽  
Fetal Circulation

The ductus arteriosus (DA) is a physiologic vessel crucial for fetal circulation. As a major regulating factor, the prostaglandin pathway has long been the target for DA patency maintenance or closure. However, the adverse effect of prostaglandins and their inhibitors has been a major unsolved clinical problem. Furthermore, a significant portion of patients with patent DA fail to respond to cyclooxygenase inhibitors that target the prostaglandin pathway. These unresponsive medical patients ultimately require surgical intervention and highlight the importance of exploring pathways independent from this well-recognized prostaglandin pathway. The clinical limitations of prostaglandin-targeting therapeutics prompted us to investigate molecules beyond the prostaglandin pathway. Thus, this article introduces molecules independent from the prostaglandin pathway based on their correlating mechanisms contributing to vascular remodeling. These molecules may serve as potential targets for future DA patency clinical management.

scholarly journals Maternal Uterine Vascular Remodeling During Pregnancy

Physiology ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 58-71 ◽  
Author(s):  
George Osol ◽  
Maurizio Mandala
Keyword(s):  
Extracellular Matrix ◽  
Blood Flow ◽  
Vascular Remodeling ◽  
Normal Pregnancy ◽  
Uterine Blood Flow ◽  
Growth And Remodeling ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Uteroplacental Blood Flow ◽  
Uterine Circulation

Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.

scholarly journals A Typical Immune T/B Subset Profile Characterizes Bicuspid Aortic Valve: In an Old Status?

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Carmela R. Balistreri ◽  
Silvio Buffa ◽  
Alberto Allegra ◽  
Calogera Pisano ◽  
Giovanni Ruvolo ◽  
...  
Keyword(s):  
B Cells ◽  
Aortic Valve ◽  
Aortic Aneurysm ◽  
Thoracic Aortic Aneurysm ◽  
Molecular Mechanisms ◽  
B Lymphocyte ◽  
Valve Disease ◽  
Tricuspid Aortic Valve ◽  
Bicuspid Valve ◽  
Circulating Levels

Bicuspid valve disease is associated with the development of thoracic aortic aneurysm. The molecular mechanisms underlying this association still need to be clarified. Here, we evaluated the circulating levels of T and B lymphocyte subsets associated with the development of vascular diseases in patients with bicuspid aortic valve or tricuspid aortic valve with and without thoracic aortic aneurysm. We unveiled that the circulating levels of the MAIT, CD4+IL−17A+, and NKT T cell subsets were significantly reduced in bicuspid valve disease cases, when compared to tricuspid aortic valve cases in either the presence or the absence of thoracic aortic aneurysm. Among patients with tricuspid aortic valve, these cells were higher in those also affected by thoracic aortic aneurysm. Similar data were obtained by examining CD19+ B cells, naïve B cells (IgD+CD27−), memory unswitched B cells (IgD+CD27+), memory switched B cells (IgD−CD27+), and double-negative B cells (DN) (IgD−CD27−). These cells resulted to be lower in subjects with bicuspid valve disease with respect to patients with tricuspid aortic valve. In whole, our data indicate that patients with bicuspid valve disease show a quantitative reduction of T and B lymphocyte cell subsets. Future studies are encouraged to understand the molecular mechanisms underlying this observation and its pathophysiological significance.

CALCIUM AND VITAMIN : EFFECTS ON BONE TISSUE AND VASCULAR REMODELING (LITERATURE REVIEW)

2021 ◽  
pp. 1200-1208
Author(s):  
С. В. Булгакова ◽  
Е. В. Тренева ◽  
Н. О. Захарова ◽  
А. В. Николаева
Keyword(s):  
Literature Review ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Vascular Wall ◽  
Arterial Calcification ◽  
Mineral Density ◽  
Treatment And Prevention ◽  
Calcium Deposits ◽  
Local Accumulation ◽  
Progression Of Atherosclerosis

Препараты кальция входят в схемы лечения и профилактики низкой минеральной плотности костной ткани. Однако последние научные исследования показали, что дополнительное поступление кальция может увеличить риск сердечно-сосудистых заболеваний. Это связано с отложением кальция в эндотелии кровеносных сосудов. Значимость минерализации сосудистой стенки не ограничивается локальным накоплением кальциевых депозитов, но в значительной мере определяется их активирующим влиянием на прогрессирование атеросклероза. Витамин К играет важную роль в гомеостазе кальция, снижает артериальную кальцификацию и артериальную жесткость и, как следствие, оказывает протективный эффект при приеме кальция. В данном обзоре литературы представлена современная информация о кальциевом парадоксе, обсуждаются основные молекулярные механизмы кальцификации сосудов, рассмотрены терапевтические стратегии лечения витамином К . Calcium preparations are included in the treatment and prevention regimens for low bone mineral density. However, recent scientific studies have shown that additional calcium intake can increase the risk of heart disease, which is associated with the deposition of calcium in the endothelium of blood vessels. The significance of vascular wall mineralization is not limited to local accumulation of calcium deposits, but is largely determined by their activating effect on the progression of atherosclerosis. Vitamin K plays an important role in calcium homeostasis, reduces arterial calcification and arterial stiffness and, as a result, has a protective effect when taking calcium. This literature review provides current information about the calcium paradox, discusses the main molecular mechanisms of vascular calcification, and considers therapeutic strategies for vitamin К treatment.

Abstract 14880: Single-cell Transcriptomes Identify Unique Endothelial Subpopulation (FABP4 + TMEM100 - ) With Lipid Metabolism Dysfunction in Pulmonary Arterial Hypertension

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
BIN LIU ◽  
Jingbo Dai ◽  
Li Shuai ◽  
Dan Yi ◽  
Youyang Zhao ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Single Cell ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Premature Death ◽  
Right Heart Failure ◽  
Fatty Acid Binding ◽  
Pulmonary Arterial ◽  
Endothelial Plasticity

Introduction: Pulmonary arterial hypertension (PAH) is a disaster disease characterized by obliterative vascular remodeling and persistent increase of vascular resistance, leading to right heart failure and premature death. Understanding the cellular and molecular mechanisms will help develop novel therapeutic approaches for PAH patients. Hypothesis: We hypothesis that endothelial plasticity or distinct cell populations are critical for obstructive vascular remodeling in the pathogenesis of PAH. Methods: Here we applied single-cell RNA sequencing (ScRNA-seq) to profile the pulmonary cells in a severe mouse model ( Egln1 Tie2Cre mice) of PAH. Human hPAEC from idiopathic PAH patients and healthy donors were used to measure FABP4 and FABP5 expression. siRNA mediated knockdown of FABP4 and FABP5 was performed to study cell proliferation and apoptosis. Mice with Fabp4 and Fabp5 deletion ( Fabp45 -/- ) and wild type (WT) mice were incubated with hypoxia (10% O 2 ) to induced PAH. Egln1 Tie2Cre mice were bred with Fabp45 -/- mice to generate Egln1 Tie2Cre / Fabp45 -/- mice. Results: We identified five distinct EC subpopulations in both WT and Egln1 Tie2Cre mice via scRNA-seq. Unexpectedly, the number of Cluster (EC2, 49.8%) was markedly increased in Egln1 Tie2Cre lung compared with WT lung (2.8%). EC2 cluster (mainly from Egln1 Tie2Cre lung) was characterized by little expression of Tmem100 , Cldn5 , Tspan7 , Calcrl and Foxf1 and high expression of Fabp4, Cdh13, Sparl1 and Fabp5 . Fatty acid-binding protein (FABP) 4 and FABP5 (FABP4-5) were highly induced in PAECs from IPAH patients. Knockdown of FABP4-5 reduced EC proliferation and starvation-induced Caspase 3/7 activity. Fabp45 -/- mice were protected from hypoxia-induced PAH compared to WT mice. Moreover, Egln1 Tie2Cre / Fabp45 -/- mice also exhibited a reduction of RVSP and RV hypertrophy compared to Egln1 Tie2Cre mice. Conclusions: ScRNA-seq analysis identifies a unique endothelial population (FABP4 + TMEM100 - ) highly enriched in the lung of severe PAH mice. Knockdown of FABP4-5 reduces EC proliferation starvation-induced injury. Genetic deletion of FABP4-5 protects from hypoxia and Egln1 deficiency-induced PAH in mice.

221. Localisation of relaxin receptors (Rxfp1) in the uterine artery and the effects of blocking circulating relaxin on passive mechanical wall properties in the uterine artery of late pregnant rats

2008 ◽  
Vol 20 (9) ◽  
pp. 21
Author(s):  
L. A. Vodstrcil ◽  
J. Novak ◽  
M. Tare ◽  
M. E. Wlodek ◽  
L. J. Parry
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Uterine Artery ◽  
Late Pregnancy ◽  
Artery Wall ◽  
Pregnant Rats ◽  
Uterine Arteries ◽  
Wall Properties ◽  
Wall Stiffness

During pregnancy, the uteroplacental circulation undergoes dramatic alterations to allow for the large increase in blood flow to the feto-placental unit. These alterations are achieved through several mechanisms including structural changes in the uterine artery wall and endothelium-dependent vasodilation. Small renal arteries of relaxin-deficient mice and rats have enhanced myogenic reactivity and decreased passive compliance, and are relatively vasoconstricted (Novak et al. 2001, 2006). To date, no study has identified relaxin receptors (Rxfp1) in arteries or investigated the effects of relaxin deficiency in pregnancy on uterine artery function. The aims of this current study were to: 1) localise Rxfp1 in the uterine arteries, 2) measure myogenic reactivity in small uterine arteries after relaxin treatment, and 3) test the hypothesis that blocking circulating relaxin in late pregnancy will increase uterine artery wall stiffness. We demonstrated that Rxfp1 is expressed in the uterine arteries of pregnant mice and rats. Brightfield immunohistochemistry and immunofluorescence using antibodies specific for rat Rxfp1, α-smooth muscle actin and CD31 localised Rxfp1 protein predominantly to the vascular smooth muscle in the uterine artery of pregnant rats. Administration of recombinant human H2 relaxin (4 ug/h) for 6 h or 5 days in intact and ovariectomised rats reduced myogenic reactivity of small uterine arteries in vitro. Pregnant rats were treated with a monoclonal antibody against circulating relaxin (MCA1) or control (MCAF) for 3 days (Days 17–19) and uterine arteries were mounted on a pressure myograph to assess passive mechanical wall properties. Neutralising circulating relaxin in late pregnancy resulted in a significant increase in uterine artery wall stiffness. These data demonstrate that relaxin acts on the vascular smooth muscle cells in the uterine artery and may be involved in the pregnancy-specific vascular remodelling of uterine arteries to increase vasodilation and blood flow to the uterus and placenta. (1) Novak J et al. (2001). J Clin Invest 107: 1469–75 (2) Novak J et al. (2006). FASEB J 20: 2352–62

Sign in / Sign up

Export Citation Format

Share Document