A study of endothelial and platelet microvesicles across different hypertension phenotypes.
Journal
Journal of human hypertension
ISSN: 1476-5527
Titre abrégé: J Hum Hypertens
Pays: England
ID NLM: 8811625
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
13
01
2021
accepted:
22
03
2021
revised:
05
03
2021
pubmed:
11
4
2021
medline:
28
6
2022
entrez:
10
4
2021
Statut:
ppublish
Résumé
Rather than being mere biomarkers reflecting generalized vascular injury, endothelial- (EMVs) and platelet-derived (PMVs) microvesicles have emerged as potent regulators of intercellular communication with significant biologic effects in vascular homeostasis and several pathophysiological responses including inflammation and thrombosis. So far, studies in hypertension are scarce, whereas no studies exist in masked hypertension (MH). We measured EMVs and PMVs in untreated, newly diagnosed hypertensives (HTs) and MHs compared to normotensive controls (NTs), and associated them with various cardiovascular risk factors. Sustained hypertension (SHT) and MH were defined according to standard blood pressure (BP) criteria. All HTs were free of cardiovascular disease and medications. Microvesicles' quantitation and detection were performed by flow cytometry by using cell-specific antibodies and corresponding isotypes (anti-CD105 and anti-CD144 for EMVs, anti-CD42a for PMVs, and Annexin V-fluorescein isothiocyanate for all microvesicles). In this study, we included 59 HTs (44 SHTs and 15 MHs) and 27 NTs. HTs had significantly elevated EMVs (p = 0.004), but not PMVs compared to NTs. MHs had significantly elevated EMVs compared to NTs (p = 0.012) but not compared to SHTs. Furthermore, EMVs significantly correlated with ambulatory (r = 0.214-0.284), central BP (r = 0.247-0.262), and total vascular resistance (r = 0.327-0.361). EMVs are increased not only in SHTs but also in MHs, a hypertension phenotype with a cardiovascular risk close to SHT. EMVs have emerged as active contributors to thromboinflammation and vascular damage and may explain, in part, the adverse cardiovascular profile of SHTs and MHs.
Identifiants
pubmed: 33837293
doi: 10.1038/s41371-021-00531-6
pii: 10.1038/s41371-021-00531-6
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
561-569Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature Limited.
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