University of Surrey

Test tubes in the lab Research in the ATI Dance Research

Release of endothelial microparticles in patients with arterial hypertension, hypertensive emergencies and catheter-related injury

Sansone, Roberto, Baaken, Maximilian, Horn, Patrick, Schuler, Dominik, Westenfeld, Ralf, Amabile, Nicolas, Kelm, Malte and Heiss, Christian (2018) Release of endothelial microparticles in patients with arterial hypertension, hypertensive emergencies and catheter-related injury Atherosclerosis, 273. pp. 67-74.

[img] Text
Release of endothelial microparticles.docx - Accepted version Manuscript

Download (105kB)
[img] Text (Graphical abstract)
Release of endothelial microparticles - Graphical abstract.docx - Supplemental Material

Download (136kB)


Background and aims

Circulating endothelial microparticles (EMPs) are increased in arterial hypertension. The role of physicomechanical factors that may induce EMP release in vivo is still unknown. We studied the relationship of EMPs and physicomechanical factors in stable arterial hypertension and hypertensive emergencies, and investigated the pattern of EMP release after mechanical endothelial injury.


In a pilot study, 41 subjects (50% hypertensives) were recruited. EMPs were discriminated by flow-cytometry (CD31+/41-, CD62e+, CD144+). Besides blood pressure measurements, pulse-wave-analysis was performed. Flow-mediated dilation (FMD), nitroglycerin-mediated dilation (NMD), and wall-shear-stress (WSS) were measured ultrasonographically in the brachial artery; microvascular perfusion by laser-Doppler ( NCT02795377). We studied patients with hypertensive emergencies before and 4 h after BP lowering by urapidil (n = 12) and studied the release of EMPs due to mechanical endothelial injury after coronary angiography (n = 10).


Hypertensives exhibited increased EMPs (CD31+/41-, CD144+, CD62e+) as compared to normotensives and EMPs univariately correlated with systolic BP (SBP), augmentation index, and pulse wave velocity and inversely with FMD. CD31+/41--EMPs correlated with diameter and inversely with WSS and NMD. CD62e+ and CD144+-EMPs inversely correlated with microvascular function. During hypertensive emergency, only CD62e+ and CD144+-EMPs were further elevated and FMD was decreased compared to stable hypertensives. Blood pressure lowering decreased CD62e+ and CD144+-EMPs and increased FMD. CD31+/41—EMPs, diameter, and WSS remained unaffected. Similar to hypertensive emergency, catheter-related endothelial injury increased only CD144+ and CD62e+-EMPs.


EMP release in hypertension is complex and may involve both physicomechanical endothelial injury and activation (CD144+, CD62e+) and decreased wall shear stress (CD31+/41-).

Graphical abstract

In arterial hypertension, increased systolic blood pressure and decreased wall shear stress (due to greater arterial diameter) are associated with the release of endothelial microparticles (EMPs). We linked this with distinct patterns of mechanical injury, activation, and endothelial dysfunction (CD62e+ and CD144+-EMPs) and decreased endothelial protection (CD31+/41--EMPs), respectively. EMPs may be part of a vicious self-perpetuating cycle involving endothelial dysfunction.

Item Type: Article
Divisions : Faculty of Health and Medical Sciences > School of Biosciences and Medicine
Authors :
Sansone, Roberto
Baaken, Maximilian
Horn, Patrick
Schuler, Dominik
Westenfeld, Ralf
Amabile, Nicolas
Kelm, Malte
Date : 12 April 2018
DOI : 10.1016/j.atherosclerosis.2018.04.012
Copyright Disclaimer : © 2018 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license.
Uncontrolled Keywords : Cell-derived microparticles; Endothelial function; Arterial hypertension; Endothelial function; Wall shear stress
Depositing User : Clive Harris
Date Deposited : 31 May 2018 07:21
Last Modified : 13 Apr 2019 02:08

Actions (login required)

View Item View Item


Downloads per month over past year

Information about this web site

© The University of Surrey, Guildford, Surrey, GU2 7XH, United Kingdom.
+44 (0)1483 300800