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Endothelin-1 decreases microvessel permeability after endothelial activation
Gregory P Victorino1, Christopher R Newton, Brian Curran
1Department of Surgery, University of California-East Bay, Oakland, California 94602, USA. victorinog@surgery.ucsf.edu
The Journal of Trauma
|June 10, 2004
Summary
Endothelin-1 (ET-1) reduces microvascular permeability in inflamed vessels. This vasoconstrictor may help decrease fluid loss in shock and sepsis, offering a potential therapeutic target.
Area of Science:
- Physiology
- Pharmacology
- Vascular Biology
Background:
- Endothelin-1 (ET-1) is a potent vasoconstrictor released during shock and sepsis.
- ET-1's role in modulating elevated microvascular permeability in activated endothelium was investigated.
Purpose of the Study:
- To determine the effect of ET-1 on hydraulic permeability (Lp) in microvessels.
- To assess ET-1's impact on endothelial activation-induced permeability.
Main Methods:
- Hydraulic permeability (Lp) measured using the Landis micro-occlusion technique.
- Paired Lp measurements before and after perfusion with varying ET-1 doses (2.0-2,000 pg/mL).
- Endothelial activation induced by adenosine triphosphate (ATP) or bradykinin, followed by ET-1 perfusion.
Main Results:
- ET-1 significantly decreased Lp at doses of 20, 200, and 2,000 pg/mL.
- ATP and bradykinin increased Lp significantly.
- ET-1 attenuated the increased Lp caused by ATP and bradykinin.
Conclusions:
- ET-1 reduced microvascular permeability in inflamed vessels.
- ET-1 may decrease third-space fluid loss in pathophysiologic states.
- ET-1's receptor-mediated function presents a target for pharmacologic manipulation.