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Department of Medical Physics and Cardiovascular Research Institute, Academic Medical Center, University of Amsterdam, 1100 DE Amsterdam, The Netherlands
Submitted 21 October 2003 ; accepted in final form 9 February 2004
The hypothesis was tested that pressure and pressure pulsation modulate vascular remodeling. Arterioles (
200 µm lumen diameter) were dissected from rat cremaster muscle and studied in organoid culture. In the first series, arterioles were kept at a stable pressure level of either 50 or 100 mmHg for 3 days. Both groups showed a progressive increase in myogenic tone during the experiment. Arterioles kept at 50 mmHg showed larger endothelium-dependent dilation, compared with vessels kept at 100 mmHg on day 3. Remodeling, as indicated by the reduction in maximally dilated diameter at 100 mmHg, was larger in arterioles kept at 50 mmHg compared with 100 mmHg: 34 ± 4.5 versus 10 ± 4.8 µm (P < 0.05). In the second series, arterioles were subjected to a stable pressure of 60 mmHg or oscillating pressure of 60 ± 10 mmHg (1.5 Hz) for 4 days. Pressure pulsation induced partial dilation and was associated with less remodeling: 34 ± 4.0 versus 19 ± 4.5 µm (P < 0.01) for stable pressure versus oscillating pressure. Vasomotion was frequently observed in all groups, and inward remodeling was larger in vessels with vasomotion: 30 ± 2.5 µm compared with vessels that did not exhibit vasomotion: 8.0 ± 5.0 µm (P < 0.01). In conclusion, these results indicate that remodeling is not enhanced by high pressure. Pressure pulsation causes partial dilation and reduces inward remodeling. The appearance of vasomotion is associated with enhanced inward remodeling.
myogenic regulation; vascular adaptation; hypertension
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