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Related Concept Videos

Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
Hypertension III: Clinical Manifestations and Diagnostic Studies01:30

Hypertension III: Clinical Manifestations and Diagnostic Studies

Hypertension is asymptomatic and also referred to as the "silent killer" until it progresses to a severe stage or causes target organ disease. Patients may experience symptoms stemming from the strain on blood vessels and tissues in various organs or the heart's increased workload.Physical exams might show no abnormalities other than high blood pressure. Signs of vascular damage, when present, correspond to the organs supplied by the affected vessels, leading to target organ damage. For...
Portal Hypertension01:22

Portal Hypertension

Portal hypertension is an increase in blood pressure within the portal venous system. Normally, this pressure is less than 5 mmHg. It is considered clinically significant when it rises above 10 mmHg. At this threshold, complications from altered blood flow and venous congestion emerge.EtiologyPortal hypertension arises from conditions that impede blood flow through the liver. The most common cause is cirrhosis, in which chronic liver injury leads to fibrotic scarring. This fibrosis narrows or...
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Related Experiment Video

Updated: May 9, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
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Published on: January 26, 2024

[Endothelial dysfunction in pregnancies with chronic hypertension].

J Procházková1, M Procházka, L Slavík

  • 1Hemato-onkologická klinika FN a LF UP, Olomouc. jana.prochazkova@fnol.cz

Ceska Gynekologie
|July 23, 2013
PubMed
Summary

This study identified key markers of endothelial activation, including von Willebrand Factor (vWF) and Plasminogen Activator Inhibitor-1 (PAI-1), which are elevated in pregnancies complicated by chronic hypertension, highlighting potential endothelial damage.

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Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
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Last Updated: May 9, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
05:31

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Published on: January 26, 2024

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
06:35

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Area of Science:

  • Obstetrics and Gynecology
  • Cardiovascular Physiology
  • Maternal-Fetal Medicine

Background:

  • Endothelial dysfunction is a critical factor in hypertensive disorders of pregnancy.
  • Identifying reliable markers of endothelial activation is crucial for monitoring pregnancy complications.
  • Physiological pregnancy involves dynamic changes in endothelial function.

Purpose of the Study:

  • To identify endothelial activation markers indicative of endothelial damage in physiological pregnancies.
  • To establish endothelial activation markers that differentiate normal pregnancies from those with chronic hypertension.

Main Methods:

  • Study involved 298 pregnant women, divided into physiological and chronic hypertension groups.
  • Blood samples were collected at three trimesters (beginning, 24-28 weeks, 36 weeks).
  • Assessed markers included t-PA, PAI-1, vWF, ePCR, MMP-2,9, TIMP-2, and endothelial microparticles using ELISA, EIA, and flow cytometry.

Main Results:

  • Significantly elevated levels of von Willebrand Factor (vWF) activity and antigen, thrombomodulin, and PAI-1 were observed in women with chronic hypertension compared to physiological pregnancies across all trimesters.
  • These findings indicate increased endothelial activation in hypertensive pregnancies.
  • No statistically significant changes were noted in other investigated parameters.

Conclusions:

  • Significant signs of endothelial dysfunction and activation are present in women with pre-existing hypertension during pregnancy.
  • Elevated vWF, thrombomodulin, and PAI-1 serve as key indicators of endothelial activation in hypertensive pregnancies.
  • Strict monitoring of pregnant women with hypertensive disease is essential.