Role of Endothelin-1 in Flow-mediated Dilatation
NCT02086253 · Status: COMPLETED · Phase: NA · Type: INTERVENTIONAL · Enrollment: 8
Last updated 2015-03-24
Summary
Endothelial dysfunction of conduit arteries contributes to the increased morbidity and cardiovascular mortality in patients with essential hypertension and appears increasingly as an independent therapeutic target. We have shown previously that besides a decrease in the availability of NO and other endothelium-derived vasodilators factors, the epoxyeicosatrienoic acids, an increase in the vasoconstrictor endothelin-1 (ET-1) may play a role in the pathophysiology of this endothelial dysfunction. Indeed, the local concentrations of endothelin-1 during the endothelium-dependent dilation of the radial artery in response to a sustained increase in blood flow decreased significantly in healthy volunteers controls but not in hypertensive patients. This lack of adaptation of the endothelinergic system could be due to a decreased clearance of endothelin-1 by endothelial ETB receptors, potentiating the vasoconstrictor action of endothelin-1 mediated by ETA receptor activation at the muscular level. However, to validate this hypothesis , it is needed to demonstrate the physiological role of ETA receptor and ETB in sustained flow-mediated dilatation of conduit arteries.
Conditions
- Healthy Conditions
Interventions
- DRUG
-
BQ-788 and/or BQ-123
Sponsors & Collaborators
-
University Hospital, Rouen
lead OTHER
Principal Investigators
-
Robinson JOANNIDES, Doctor · Chu - Hôpitaux de Rouen
Study Design
- Allocation
- RANDOMIZED
- Masking
- NONE
- Model
- CROSSOVER
Eligibility
- Min Age
- 18 Years
- Max Age
- 35 Years
- Sex
- MALE
- Healthy Volunteers
- Yes
Timeline & Regulatory
- Start
- 2014-02-28
- Primary Completion
- 2014-05-31
- Completion
- 2014-05-31
Countries
- France
Study Locations
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