Hypertension is a risk factor for many cardiovascular and cerebrovascular
diseases such as atherosclerosis and stroke. It is therefore important to understand the
effect of hypertension on temporal growth and remodeling of arteries. In this study,
experimental hypertension was induced in the mini-pig by aortic coarctation. Basilar
arteries and aortas were collected for analysis over an eight week period of hypertension
with specimens from normotensive animals serving as controls. Changes in mechanical
properties of the basilar artery were evaluated by in vitro pressure-diameter tests on
intact cylindrical segments at their in situ length. The basilar arteries from hypertensive
animals became less distensible, reflecting increases in both structural and material
stiffness, compared to their normotensive counterparts. The circumferential stress
rapidly returned toward its homeostatic value by increasing the wall thickness within
two weeks. Immunohistochemistry, which is capable of illustrating the localization and
distribution of protein expression, was performed to examine changes in wall
constituents in the aorta. The increased medial thickness observed in hypertensive pigs
compared to normotensive pigs was due to hyperplasia of smooth muscle cells (SMCs)
and accumulation of extracellular matrix proteins, which were accompanied by the phenotypic modulation of SMCs. The increased interlamellar thickness, collagen fibers,
and the thickness of elastic lamina found in the inner media of hypertensive animal may
be associated with the gradient of stress decreasing into the outer media. SMC
proliferation, if any, was found evenly distributed across the media, however. In cases
showing increased proliferation and matrix protein synthesis, the SMC contractile
markers were down-regulated whereas the SMC synthetic markers were up-regulated.
While the aortic intima appeared normal in the normotensive animals, neointima
formation, which may predispose the vessel to atheroma formation, was found in the
hypertensive animals. Immunohistochemistry of Hsp47 and procollagen revealed that
the endothelial cells (ECs) may produce collagen, specifically type I collagen in
response to hypertension and contribute to the thickened intima. In addition, lectin
staining for ECs markers and immunostaining for eNOS suggested that endothelial cells
may transdifferentiate into intimal SMCs. These findings suggested an alternative role
that ECs may play in hypertension-induced atherogenesis.
| Identifer | oai:union.ndltd.org:tamu.edu/oai:repository.tamu.edu:1969.1/4982 |
| Date | 25 April 2007 |
| Creators | Hu, Jin-Jia |
| Contributors | Humphrey, Jay D. |
| Publisher | Texas A&M University |
| Source Sets | Texas A and M University |
| Language | en_US |
| Detected Language | English |
| Type | Book, Thesis, Electronic Dissertation, text |
| Format | 4020132 bytes, electronic, application/pdf, born digital |
Page generated in 0.0018 seconds