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Arterial remodeling in chronic sinoaortic-denervated rats
1Department of Pharmacology, Basic Medical College, Second Military Medical University, Shanghai, China. cymiao@citiz.net
Journal of Cardiovascular Pharmacology
|January 11, 2001
Summary
Chronic sinoaortic denervation in rats significantly increases blood pressure variability (BPV) and causes vascular remodeling. This remodeling may involve increased aortic angiotensin II and altered arterial function, potentially linked to high BPV.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Renal Physiology
Background:
- Blood pressure variability (BPV) refers to spontaneous blood pressure fluctuations.
- The chronic sinoaortic-denervated (SAD) rat model exhibits high BPV without sustained hypertension.
- Vascular remodeling in SAD rats remains poorly understood.
Purpose of the Study:
- To investigate blood pressure, vascular remodeling, and aortic angiotensin II levels in chronic SAD rats.
- To characterize structural and functional arterial changes following sinoaortic denervation.
- To explore the relationship between BPV, vascular remodeling, and the tissue renin-angiotensin system.
Main Methods:
- Continuous intra-arterial blood pressure recording in conscious rats.
- Histological analysis and computer imaging for arterial structural assessment.
- Isolated artery preparations for functional evaluation and radioimmunoassay for angiotensin II quantification.
Main Results:
- SAD rats showed significantly increased BPV over 24 hours, with no change in mean blood pressure.
- Vascular remodeling included increased arterial wall thickness, wall area, and wall-to-lumen ratio, indicative of vascular growth.
- Aortic contraction to norepinephrine was potentiated, and relaxation to acetylcholine was attenuated; aortic angiotensin II increased, while plasma levels remained unchanged.
Conclusions:
- Chronic sinoaortic denervation induces significant vascular remodeling in rats.
- This remodeling is associated with increased BPV and elevated aortic angiotensin II.
- The findings suggest an activated tissue renin-angiotensin system contributes to vascular changes and high BPV in SAD rats.