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Improvement in middle cerebral artery structure and endothelial function in stroke-prone spontaneously hypertensive
Paulo W Pires1, Saavia S Girgla, Jonathon L McClain
1Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan, USA.
Background:
Inflammation is involved in the pathogenesis of hypertension. Hypertensive animals have an increased number of perivascular macrophages in cerebral arteries. Macrophages might be involved in remodeling of the cerebral vasculature. We hypothesized that peripheral macrophage depletion would improve MCA structure and function in hypertensive rats.
Methods:
For macrophage depletion, six-week-old stroke-prone spontaneously hypertensive rats (SHRSP) were treated with CLOD, 10 mL/kg every three or four days, i.p., or vehicle (PBS lipo). MCA structure and function were analyzed by pressure and wire myography.
Results:
Blood pressure was not affected by CLOD. The number of perivascular CD163-positive cells per microscopic field was reduced in the brain of SHRSP+CLOD. CLOD treatment caused an improvement in endothelium-dependent dilation after intralumenal perfusion of ADP and incubation with Ach. Inhibition of NO production blunted the Ach response, and endothelium-independent dilation was not altered. At an intralumenal pressure of 80 mmHg, MCA from SHRSP+CLOD showed increased lumen diameter, decreased wall thickness, and wall-to-lumen ratio. Cross-sectional area of pial arterioles from SHRSP+CLOD was higher than PBS lipo.
Conclusions:
These results suggest that macrophage depletion attenuates MCA remodeling and improves MCA endothelial function in SHRSP.
Insights
Depleting macrophages in hypertensive rats improved cerebral artery structure and function, reducing vascular remodeling. This suggests targeting macrophages may be a therapeutic strategy for hypertension-related vascular changes.
Area of Science:
- Cardiovascular Science
- Neuroscience
- Immunology
Background:
- Inflammation plays a key role in hypertension development.
- Hypertensive rats exhibit increased perivascular macrophages in cerebral arteries.
- Macrophages may contribute to cerebral vascular remodeling.
Purpose of the Study:
- To investigate if peripheral macrophage depletion impacts cerebral artery structure and function in hypertensive rats.
- To test the hypothesis that reducing macrophages improves MCA remodeling.
Main Methods:
- Stroke-prone spontaneously hypertensive rats (SHRSP) were treated with clodronate (CLOD) or vehicle (PBS lipo).
- Macrophage depletion was confirmed by reduced CD163-positive cells.
- Middle cerebral artery (MCA) structure and function were assessed using pressure and wire myography.
Main Results:
- CLOD treatment did not affect blood pressure but reduced perivascular macrophages.
- Endothelium-dependent vasodilation improved in CLOD-treated rats.
- MCA showed increased lumen diameter, decreased wall thickness, and reduced wall-to-lumen ratio.
Conclusions:
- Macrophage depletion attenuates MCA remodeling in hypertensive rats.
- Peripheral macrophage depletion improves MCA endothelial function.
- Targeting macrophages may offer a therapeutic approach for hypertension-associated vascular dysfunction.
