| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Medical Physics and Cardiovascular Research Institute (CRIA), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
* To whom correspondence should be addressed. E-mail: n.t.bakker{at}amc.uva.nl.
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 mmHg 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 endotheliumdependent dilation, as compared to 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 as compared to 100 mmHg: 34 ± 4.5 µm vs. 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 µm vs. 19 ± 4.5 µm (p<0.01) for stable pressure vs. oscillating pressure. Vasomotion was frequently observed in all groups, and inward remodeling was larger in vessels with vasomotion: 30 ± 2.5 µm as compared to 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.
This article has been cited by other articles:
|
|
 |
|
  J. C. B. Jacobsen, M. J. Mulvany, and N.-H. Holstein-Rathlou A mechanism for arteriolar remodeling based on maintenance of smooth muscle cell activation Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2008; 294(4): R1379 - R1389. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Sorop, E. N. T. P. Bakker, A. Pistea, J. A. E. Spaan, and E. VanBavel Calcium channel blockade prevents pressure-dependent inward remodeling in isolated subendocardial resistance vessels Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1236 - H1245. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. de Waard, E. K. Arkenbout, M. Vos, A. I.M. Mocking, H. W.M. Niessen, W. Stooker, B. A.J.M. de Mol, P. H.A. Quax, E. N.T.P. Bakker, E. VanBavel, et al. TR3 Nuclear Orphan Receptor Prevents Cyclic Stretch-Induced Proliferation of Venous Smooth Muscle Cells Am. J. Pathol., June 1, 2006; 168(6): 2027 - 2035. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Pistea, E. N. T. P. Bakker, J. A. E. Spaan, and E. VanBavel Flow inhibits inward remodeling in cannulated porcine small coronary arteries Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2632 - H2640. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. R. De Mey, P. M. Schiffers, R. H. P. Hilgers, and M. M. W. Sanders Toward functional genomics of flow-induced outward remodeling of resistance arteries Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1022 - H1027. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
