Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Sep 11;31(10):1067-1078.
doi: 10.1093/ajh/hpy083.

Hypertension Induced Morphological and Physiological Changes in Cells of the Arterial Wall

Affiliations
Review

Hypertension Induced Morphological and Physiological Changes in Cells of the Arterial Wall

Patricia Martinez-Quinones et al. Am J Hypertens. .

Abstract

Morphological and physiological changes in the vasculature have been described in the evolution and maintenance of hypertension. Hypertension-induced vascular dysfunction may present itself as a contributing, or consequential factor, to vascular remodeling caused by chronically elevated systemic arterial blood pressure. Changes in all vessel layers, from the endothelium to the perivascular adipose tissue (PVAT), have been described. This mini-review focuses on the current knowledge of the structure and function of the vessel layers, specifically muscular arteries: intima, media, adventitia, PVAT, and the cell types harbored within each vessel layer. The contributions of each cell type to vessel homeostasis and pathophysiological development of hypertension will be highlighted.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Arterial remodeling in hypertension. Typical representative images of mesenteric resistance arteries from Wistar–Kyoto (WKY) and spontaneously hypertensive rats (SHR) showing the inward remodeling in SHR arteries. Confocal images (×40 magnification) of increased colocalization immunofluorescence for Toll-like receptor 9 (red) and MyD88 (green).
Figure 2.
Figure 2.
Identification of pericytes in mice renal medullary capillaries. Pericytes (arrow) wrapping around medullary renal capillaries. Nerve/glial antigen 2-NG2 (red) used as pericyte localization marker for immunofluorescence. Abbreviation: DAPI (blue), 4′,6-diamidino-2-phenylindole.
Figure 3.
Figure 3.
Representative images comparing vascular changes between resistance arteries from normotensive (a) and hypertensive (b) model. When comparing hypertensive resistance arteries with normotensive ones, it is important to note that endothelial cells are damaged and express adhesion molecules, VSMC hypertrophy and hyperplasia, increase in number of infiltrating cells between the medial layer and adventitial layer, increased collagen deposition, and increased number of resident fibrocytes.

Similar articles

Cited by

References

    1. Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA, Williamson JD, Wright JT. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/ PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines, 2017.
    1. Fry DL. Acute vascular endothelial changes associated with increased blood velocity gradients. Circ Res 1968; 22:165–197. - PubMed
    1. Fry DL. Certain histological and chemical responses of the vascular interface to acutely induced mechanical stress in the aorta of the dog. Circ Res 1969; 24:93–108. - PubMed
    1. Vaziri ND, Ni Z, Oveisi F. Upregulation of renal and vascular nitric oxide synthase in young spontaneously hypertensive rats. Hypertension 1998; 31:1248–1254. - PubMed
    1. Wenceslau CF, McCarthy CG, Szasz T, Goulopoulou S, Webb RC. Mitochondrial N-formyl peptides induce cardiovascular collapse and sepsis-like syndrome. Am J Physiol Heart Circ Physiol 2015; 308:H768–H777. - PMC - PubMed

Publication types