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Not Yet RecruitingNCT06316271

Endothelial Function in Prehypertension

Endothelial Dysfunction and Cardiovascular Remodeling in Pathophyisiology of Prehypertension

Status
Not Yet Recruiting
Phase
Study type
Observational
Enrollment
90 (estimated)
Sponsor
Josip Juraj Strossmayer University of Osijek · Academic / Other
Sex
All
Age
18 Years – 69 Years
Healthy volunteers
Accepted

Summary

In the frame of this proposal investigators will test the hypothesis that high normal blood pressure (prehypertension; PreHT) induces systemic endothelial dysfunction and endothelial activation in both micro- and macrocirculation, reduces re-endothelialization potential of human endothelial progenitor cells (EPCs) and increases the level of endothelial extracellular vesicles (EVs), which are accompanied by increased oxidative stress level. Furthermore, initial vascular and left ventricle (LV) remodeling contributes to changes in systemic hemodynamics and may be influenced by altered regulatory role of renin-angiotensin system (RAS) and autonomic nervous system (ANS) in PreHT but otherwise healthy individuals. To distinguish high normal blood pressure effect from those considered normal or high, study will be performed in three groups of individuals: prehypertensive (BP 130-139/85-89 mmHg), hypertensive (stage I, BP 140-150/90-100 mmHg), and controls (BP less than or equal to 129/85 mmHg). Altogether, the impairment of normal vascular relaxation mechanisms, endothelial activation as well as vascular and LV remodeling could play crucial role in increased cardiovascular risk and CVDs incidence in PreHT individuals. Moreover, the prognostic significance of assessing endotehlial dysfunction in hypertension (as well as in PreHT) is yet to be established.

Conditions

Timeline

Start date
2024-04-01
Primary completion
2024-12-31
Completion
2026-12-31
First posted
2024-03-18
Last updated
2024-03-18

Locations

1 site across 1 country: Croatia

Source: ClinicalTrials.gov record NCT06316271. Inclusion in this directory is not an endorsement.