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Cerebrovascular permeability in mechanically induced hypertension
Summary
Acute hypertension, regardless of cause, increases cerebrovascular permeability primarily through enhanced pinocytosis. This study confirms that the hypertensive state, not angiotensin itself, drives these changes in blood vessels of the brain.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Cell Biology
Background:
- Previous research linked angiotensin-induced hypertension to increased cerebrovascular permeability via enhanced pinocytosis.
- The direct effect of angiotensin versus the hypertensive state on permeability remained unclear.
Purpose of the Study:
- To investigate cerebrovascular permeability changes in non-pharmacologically induced acute hypertension.
- To determine if enhanced pinocytosis is a general response to hypertension or specific to angiotensin administration.
Main Methods:
- Acute hypertension was induced in rats by aortic banding.
- Horseradish peroxidase (HRP) was administered intravenously to assess vascular permeability.
- Cerebrovascular permeability and pinocytotic activity were examined in cortical arterioles.
Main Results:
- Non-pharmacological hypertension induced similar permeability alterations as angiotensin-induced hypertension.
- Increased permeability was observed in focal segments of penetrating arterioles in the temporal and parietal cortex.
- Enhanced pinocytosis, indicated by increased vesicles, was the primary mechanism for increased permeability; interendothelial junctions remained unaltered.
Conclusions:
- Enhanced pinocytosis is the principal mechanism for increased cerebrovascular permeability during acute hypertension.
- The observed permeability alterations are a consequence of the hypertensive state itself, not a direct pharmacological effect of exogenous angiotensin.