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Remodeling of cerebral arterioles in chronic hypertension
1University of Iowa College of Medicine, Department of Pathology, Iowa City 52242.
Insights
Chronic hypertension reduces cerebral arteriole diameter by decreasing external diameter, not just wall thickening. This structural remodeling impairs blood flow regulation in hypertensive rats.
Area of Science:
- Cardiovascular Physiology
- Cerebrovascular Research
- Hypertension Pathophysiology
Background:
- Chronic hypertension is known to impair cerebral arteriole dilation.
- This impairment has been primarily attributed to arteriolar wall hypertrophy.
- The role of external diameter reduction in lumen encroachment was not well understood.
Purpose of the Study:
- To investigate if reduced external diameter contributes to lumen encroachment in cerebral arterioles during chronic hypertension.
- To differentiate the contributions of external diameter reduction and wall hypertrophy to impaired vasodilation.
Main Methods:
- Utilized Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) aged 10-12 months.
- Measured pial arteriolar pressure, diameter, and wall cross-sectional area under anesthesia.
- Calculated external diameter, stress, and strain during maximal vasodilation induced by ethylenediaminetetraacetic acid.
Main Results:
- SHRSP exhibited a greater arteriolar wall cross-sectional area compared to WKY rats.
- Both external and internal diameters of pial arterioles were significantly smaller in SHRSP.
- Reduced external diameter accounted for 76% of lumen encroachment, while hypertrophy accounted for only 24%.
Conclusions:
- Reduction in external diameter is a key factor in the impaired maximal dilation of cerebral arterioles in SHRSP.
- Altered distensibility does not explain the reduced vascular diameter in SHRSP.
- Chronic hypertension induces structural remodeling in cerebral arterioles, leading to decreased external diameter and lumen encroachment.
Abstract:
Chronic hypertension impairs dilatation of cerebral arterioles. Impairment of dilatation generally has been attributed to hypertrophy of the vessel wall with encroachment on the vascular lumen. In this study, we tested the hypothesis that a reduction in external diameter may contribute to encroachment on the vascular lumen during chronic hypertension. We examined 10-12-month-old, anesthetized Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP). External diameter, stress, and strain of pial arterioles were calculated from measurements of pial arteriolar pressure (servo null), diameter, and cross-sectional area of the arteriolar wall. During maximal dilatation produced with ethylenediaminetetraacetic acid, cross-sectional area of the arteriolar wall was greater in SHRSP than in WKY rats (2,038 +/- 57 vs. 1,456 +/- 61 micron 2, p less than 0.05). External, as well as internal, diameter was less in SHRSP than in WKY rats (101 +/- 3 and 88 +/- 3 micron in SHRSP vs. 111 +/- 3 and 102 +/- 3 micron in WKY rats for external and internal diameter, respectively, p less than 0.05). Reduction in external diameter accounted for 76% of encroachment on the lumen in SHRSP, and hypertrophy per se accounted for only 24%. Distensibility of deactivated pial arterioles was increased in SHRSP. These findings suggest that reduction in external diameter plays an important role in impairment of maximal dilatation of cerebral arterioles in SHRSP, and reduction in vascular diameter in SHRSP cannot be accounted for by altered distensibility. We propose that, during chronic hypertension, cerebral arterioles undergo structural remodeling that results in a smaller external diameter and encroachment on the vascular lumen.(ABSTRACT TRUNCATED AT 250 WORDS)