Trials / Not Yet Recruiting
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.