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A study of endothelial and platelet microvesicles across different hypertension phenotypes

Authors :
Eleni Gavriilaki
Panagiota Anyfanti
P. Dolgyras
Stella Douma
Christos Tzimos
Barbara Nikolaidou
Areti Triantafyllou
Dimitra Markala
Efi Yiannaki
Nikolaos Koletsos
Eugenia Gkaliagkousi
Antonios Lazaridis
Source :
Journal of Human Hypertension. 36:561-569
Publication Year :
2021
Publisher :
Springer Science and Business Media LLC, 2021.

Abstract

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.

Details

ISSN :
14765527 and 09509240
Volume :
36
Database :
OpenAIRE
Journal :
Journal of Human Hypertension
Accession number :
edsair.doi.dedup.....788aed21d5dd21ee563d7dacf1d24c46
Full Text :
https://doi.org/10.1038/s41371-021-00531-6