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Captopril improves cerebrovascular structure and function in old hypertensive rats.
François Dupuis1, Jeffrey Atkinson, Patrick Limiñana
1Cardiovascular Research Group, EA 3448, Faculté de Pharmacie de l'Université Henri Poincaré-Nancy I, 5 rue Albert Lebrun, 54000 Nancy, France.
British Journal of Pharmacology
|January 19, 2005
Summary
Angiotensin-converting enzyme inhibitors (ACEIs) like captopril reduce inward remodeling of cerebral arterioles in hypertensive rats. This improves cerebral blood flow autoregulation, particularly in older hypertensive subjects.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Cerebrovascular Medicine
Background:
- Hypertension is associated with structural changes in cerebral arterioles, impacting blood flow regulation.
- Angiotensin-converting enzyme inhibitors (ACEIs) are used to manage hypertension, but their specific effects on cerebral arterioles require further investigation.
Purpose of the Study:
- To investigate the impact of captopril, an ACEI, on cerebral arterioles in young and old spontaneously hypertensive rats (SHR).
- To assess how captopril influences cerebral blood flow (CBF) autoregulation and arteriolar structure under hypotensive conditions.
Main Methods:
- Cerebral blood flow and arteriolar internal diameter were measured in Wistar Kyoto rats and SHR (untreated or captopril-treated).
- Animals underwent stepwise hypotension to assess autoregulation.
- Cerebral arteriolar cross-sectional area and external diameter were measured after deactivation.
Main Results:
- Captopril treatment decreased the lower limit of cerebral blood flow autoregulation in SHR.
- ACEI treatment reduced the cross-sectional area of the cerebral arteriolar wall in SHR.
- Captopril increased cerebral arteriolar external diameter in SHR and attenuated increases in arteriolar distensibility.
Conclusions:
- ACEIs, such as captopril, attenuate inward remodeling (eutrophic and hypertrophic) of cerebral arterioles in both young and old SHR.
- This remodeling attenuation by ACEIs leads to a reduced lower limit of cerebral blood flow autoregulation.