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Angiotensin II increases vascular permeability factor gene expression by human vascular smooth muscle cells
B Williams1, A Q Baker, B Gallacher
1Department of Medicine, University of Leicester, School of Medicine, UK.
Hypertension (Dallas, Tex. : 1979)
|May 1, 1995
Summary
Angiotensin II (Ang II) increases vascular permeability by inducing vascular permeability factor (VPF) mRNA in smooth muscle cells. This action is independent of blood pressure changes, suggesting a direct endothelial effect.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Function
- Molecular Medicine
Background:
- Angiotensin II (Ang II) is linked to vascular injury in hypertension and diabetes.
- Increased vascular permeability is an early sign of endothelial dysfunction and atherosclerosis.
- The mechanism by which Ang II increases vascular permeability is not fully understood.
Purpose of the Study:
- To investigate the role of Ang II in regulating vascular permeability factor (VPF) expression in human vascular smooth muscle cells.
- To determine if Ang II directly influences endothelial permeability independent of its pressor effects.
Main Methods:
- Assessed VPF mRNA expression in human vascular smooth muscle cells treated with Ang II.
- Investigated the concentration and time-dependence of Ang II's effect on VPF mRNA.
- Utilized the Ang II receptor antagonist losartan to confirm the involvement of Ang II receptor subtype 1.
Main Results:
- Human vascular smooth muscle cells express VPF mRNA.
- Ang II significantly increased VPF mRNA expression in a dose- and time-dependent manner.
- Losartan blocked the Ang II-induced VPF mRNA expression, indicating an Ang II receptor subtype 1-mediated mechanism.
Conclusions:
- Ang II induces VPF mRNA expression in human vascular smooth muscle cells via the Ang II receptor subtype 1.
- This represents a novel mechanism for Ang II to directly affect vascular permeability and endothelial function, independent of hemodynamic changes.