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Coronary vascular hyperpermeability and angiotensin II
1Department of Internal Medicine, University of Missouri-Columbia 65212, USA.
The Journal of Laboratory and Clinical Medicine
|September 1, 1995
Summary
Elevated angiotensin II (AngII) causes coronary vascular hyperpermeability. This study shows AngII triggers prostaglandin E2 (PGE2) release and gelatinase activation, contributing to vascular leakage and fibrosis.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
Background:
- Elevated plasma angiotensin II (AngII) is linked to vascular hyperpermeability and perivascular fibrosis.
- The specific mediators driving AngII-induced hyperpermeability and fibrogenesis remain unidentified.
Purpose of the Study:
- To investigate the relationship between AngII-induced coronary hyperpermeability and the release of prostaglandin E2 (PGE2).
- To examine the activation of matrix metalloproteinase gelatinase/type IV collagenase in response to AngII.
Main Methods:
- Intravenous infusion of AngII or saline in dogs, monitoring cardiac lymph over 90 minutes.
- Analysis of lymph for total protein, albumin, fibronectin, PGE2, and gelatinase/type IV collagenase activity.
Main Results:
- AngII infusion significantly increased lymph flow, total protein, albumin, fibronectin, PGE2, and gelatinase/type IV collagenase levels.
- These changes were observed within 30 minutes of AngII administration and not in the saline control group.
Conclusions:
- Angiotensin II-induced coronary vascular hyperpermeability is associated with the early release of prostaglandin E2.
- The activation of gelatinase/type IV collagenase is also linked to AngII-induced hyperpermeability, suggesting its role in vascular remodeling.