Cited by 979Cardiac Fibrosis and RemodelingRenin-Angiotensin System StudiesCardiovascular Health and Disease Prevention

Vascular Remodeling in Hypertension: Roles of Apoptosis, Inflammation, and Fibrosis

Intengan, Hope D., Schiffrin, Ernesto L.·2001·Hypertension

Abstract

Abstract — — Remodeling of large and small arteries contributes to the development and complications of hypertension. The focus of this review is some of the mechanisms involved in the remodeling of small arteries in hypertension. In hypertension, changes in small artery structure are basically of 2 kinds: (1) inward eutrophic remodeling, in which outer and lumen diameters are decreased, media/lumen ratio is increased, and cross-sectional area of the media is unaltered; and (2) hypertrophic remodeling, in which the media thickens to encroach on the lumen, resulting in increased media cross-sectional area and media/lumen ratio. Growth, apoptosis, inflammation, and fibrosis contribute to vascular remodeling in hypertension. Apoptosis is gene-regulated cell death, with minimal membrane disruption and inflammation, that counters cell proliferation and fine-tunes developmental growth. Apoptosis has been reported in hypertension to be both increased and decreased in different tissues, including blood vessels. Inflammation, which may be low grade, probably plays an important role in triggering fibrosis in cardiovascular disease and hypertension. Vascular fibrosis entails accumulation of collagen, fibronectin, and other extracellular matrix components in the vessel wall and is an important aspect of extracellular matrix remodeling in hypertension. Associated with this, there may be increases in cell-matrix attachment sites (integrins) and changes in their topographical localization that may modulate arterial structure. Imbalance in matrix metalloproteinase/tissue inhibitors of metalloproteinases may contribute to alteration in collagen turnover and extracellular matrix remodeling. Chronic vasoconstriction may lead to embedding of the contracted vessel structure in a remodeled extracellular matrix, contributing to the inward remodeling of the blood vessel as smooth muscle cells are rearranged around a smaller lumen. The resulting remodeling of small arteries may initially be adaptive, but eventually it becomes maladaptive and compromises organ function, contributing to cardiovascular complications of hypertension.

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Crossref · 10.1161/hy09t1.096249

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Research works printed but not linked: 5

  1. Mulvany MJ, Baumbach GL, Aalkjaer C, Heagerty AM, Korsgaard N, Schiffrin EL, Heistad DD. Vascular remodeling. Hypertension. 1996;28: 505-506.
  2. Deng LY, Schiffrin EL. Morphologic and functional alterations of mes- enteric small resistance arteries in early renal hypertension in the rat. Am J Physiol. 1991;261:H1171-H1177.
  3. Kim S, Ohta K, Hamaguchi A, Omura T, Yukimura T, Miura K, Inada Y, Ishimura Y, Chatani F, Iwao H. Angiotensin II type I receptor antagonist inhibits the gene expression of transforming growth factor-␤1 and extra- cellular matrix in cardiac and vascular tissues of hypertensive rats. J Pharmacol Exp Ther. 1995;273:509 -515.
  4. Intengan HD, Schiffrin EL. Collagen degradation is diminished in mes- enteric arteries of spontaneously hypertensive rats after hypertension is established. Hypertension. 1999;34:329. Abstract.
  5. Benetos A, Lacolley P, Safar ME. Prevention of aortic fibrosis by spi- ronolactone in spontaneously hypertensive rats. Arterioscler Thromb Vasc Biol. 1997;17:1152-1156.

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Authors
Intengan, H. D., & Schiffrin, E. L.
Affiliations
University of California, San Francisco (US)
Venue
Hypertension
Published
2001-09
Volume
38
Issue
3
Pages
581-587
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
OpenAlex
W2097792029
Cited by
979
References
140
Citations by year
2026: 21 · 2025: 38 · 2024: 26 · 2023: 37 · 2022: 46 · 2021: 43 · 2020: 39 · 2019: 36 · 2018: 38 · 2017: 46 · 2016: 69 · 2015: 51 · 2014: 56 · 2013: 41 · 2012: 52
FWCI
4.40
Type
journal article
Language
en
Open access
closed
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Medical Research Council Canada
  • Canadian Institutes of Health Research (37917)
  • Medical Research Council
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
Keywords
vascular remodeling, small arteries, apoptosis, inflammation, vascular fibrosis, extracellular matrix, integrins, matrix metalloproteinases, tissue inhibitors of metalloproteinases, collagen turnover, vasoconstriction, smooth muscle cells, media-to-lumen ratio
MeSH terms
Animals, Blood Pressure, Blood Vessels, Fibrosis, Humans, Hypertension, Inflammation, Models, Biological, Apoptosis

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