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Potential Role of Antihypertensive Medications in Preventing Excessive Arterial Stiffening

  • Hypertension and the Kidney (RM Carey, Section Editor)
  • Published:
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Abstract

Purpose of Review

Increased arterial stiffness, an abnormal structural and functional change in the vascular wall, is a precursor for hypertension, coronary heart disease, stroke, and associated cardiovascular disease (CVD). The aim of this paper is to review the etiology of arterial stiffening and potential therapeutic approaches to modulate arterial fibrosis and stiffness.

Recent Findings

The Framingham Heart Study demonstrated that arterial stiffness is an independent predictor of CVD and related morbidity and mortality. Dysfunction of endothelial cells, vascular smooth muscle cells, extracellular matrix, and other functional elements of the vessel wall contribute to underlying pathophysiology of increased arterial stiffness. An activated renin-angiotensin-aldosterone system, oxidative stress, abnormal peri-vascular adipose tissue, inflammation, and increased sympathetic nervous system activity are associated with the development and progression of arterial fibrosis, stiffening, and associated CVD.

Summary

In this review, we will discuss the structural and function changes and mechanisms of the vessel wall in arterial stiffness and provide potential therapeutic strategies.

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Abbreviations

ACE:

Angiotensin converting enzyme

Ang II:

Angiotensin II

AT-1R:

Ang II receptor 1

cfPWC:

Carotid–femoral PWV

CVD:

Cardiovascular disease

EC:

Endothelial cells

ECM:

Extracellular matrix

ENaC:

Epithelial Na+ channel

EnNaC:

Endothelial ENaC

eNOS:

Endothelial NO synthase

MMPs:

Matrix metalloproteinases

MR:

Mineralocorticoid receptor

Na+ :

Sodium

NADPH:

Nicotinamide adenine dinucleotide phosphate

NF-κB:

Nuclear factor kappa B

NO:

Nitric oxide

NOX:

NADPH oxidase

PVAT:

Peri-vascular adipose tissue

PWV:

Pulse wave velocity

RAAS:

Activated renin-angiotensin-aldosterone system

ROS:

Reactive oxygen specie

SGK1:

Serum and glucocorticoid-regulated kinase 1

TGF-β1:

Transforming growth factor beta 1

VSMC:

Vascular smooth muscle cell

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Authors and Affiliations

  1. Diabetes and Cardiovascular Research Center, University of Missouri School of Medicine, D109 Diabetes Center HSC, One Hospital Drive, Columbia, MO, 65212, USA

    Guanghong Jia, Annayya R. Aroor & James R. Sowers

  2. Research Service, Truman Memorial Veterans Hospital, Columbia, MO, 65201, USA

    Guanghong Jia, Annayya R. Aroor, Luis A. Martinez-Lemus & James R. Sowers

  3. Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, 65211, USA

    Luis A. Martinez-Lemus & James R. Sowers

  4. Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, 65212, USA

    Luis A. Martinez-Lemus & James R. Sowers

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  1. Guanghong Jia
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  2. Annayya R. Aroor
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  3. Luis A. Martinez-Lemus
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  4. James R. Sowers
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Jia, G., Aroor, A.R., Martinez-Lemus, L.A. et al. Potential Role of Antihypertensive Medications in Preventing Excessive Arterial Stiffening. Curr Hypertens Rep 20, 76 (2018). https://doi.org/10.1007/s11906-018-0876-9

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