Vol 3, No 2 (1999)
REVIEV
Published online: 2000-03-08
Get Citation

The Connective Tissue of the Arterial Wall in Pathogenesis of Atherosclerosis and Hypertension

Wojciech Wojakowski, Jan Gmiński 9
Nadciśnienie tętnicze 1999;3(2):97-107.
Vol 3, No 2 (1999)
REVIEV
Published online: 2000-03-08

Abstract

In atherosclerosis numerous qualitative and quantitative changes in connective tissue metabolism parameters in serum and aorta occur. The elastin turnover is accelerated due to increased activity of elastases in serum and arterial wall. The activity of protease inhibitors is decreased. Also, the collagen's content of arterial wall was shown to be higher. Connective tissue is an important factor in regulation of smooth muscle cells (SMC) proliferation and migration, immunological processes during atherosclerosis and interactions with blond cells. The renin-angiotensin system plays an important role in atherogenesis and hypertension. Angiotensin II (ANG II) was shown to stimulate the phenotypic modulation of SMC. It induces SMC proliferation and migration from media to subendothelial layer, enhances the action of other growth factors, induces the adhesion and migration of monocytes and macrophages roto vascular wali, activates platelets and reduces fibrinolytic activity, stimulates modifications ofLDL particles and foam cells accumulation. During vascular injury there is an enhanced activity oflocal reninangiotensin system. It leads to overproduction of ANG II, both in serum and arterial wali. ANG II stimulates SMC to oversynthesize the extracellular matrix components - collagens type I and III, fibronectin, tenascin, thrombospondin, osteopontin and glycosaminoglycans - chondroitin and dermatan sulfates. It was shown that SMC under influence of ANG II synthesize less elastin.

Abstract

In atherosclerosis numerous qualitative and quantitative changes in connective tissue metabolism parameters in serum and aorta occur. The elastin turnover is accelerated due to increased activity of elastases in serum and arterial wall. The activity of protease inhibitors is decreased. Also, the collagen's content of arterial wall was shown to be higher. Connective tissue is an important factor in regulation of smooth muscle cells (SMC) proliferation and migration, immunological processes during atherosclerosis and interactions with blond cells. The renin-angiotensin system plays an important role in atherogenesis and hypertension. Angiotensin II (ANG II) was shown to stimulate the phenotypic modulation of SMC. It induces SMC proliferation and migration from media to subendothelial layer, enhances the action of other growth factors, induces the adhesion and migration of monocytes and macrophages roto vascular wali, activates platelets and reduces fibrinolytic activity, stimulates modifications ofLDL particles and foam cells accumulation. During vascular injury there is an enhanced activity oflocal reninangiotensin system. It leads to overproduction of ANG II, both in serum and arterial wali. ANG II stimulates SMC to oversynthesize the extracellular matrix components - collagens type I and III, fibronectin, tenascin, thrombospondin, osteopontin and glycosaminoglycans - chondroitin and dermatan sulfates. It was shown that SMC under influence of ANG II synthesize less elastin.
Get Citation

Keywords

elastin; collagens; elastase(s); atherosclerosis; hypertension

About this article
Title

The Connective Tissue of the Arterial Wall in Pathogenesis of Atherosclerosis and Hypertension

Journal

Arterial Hypertension

Issue

Vol 3, No 2 (1999)

Pages

97-107

Published online

2000-03-08

Bibliographic record

Nadciśnienie tętnicze 1999;3(2):97-107.

Keywords

elastin
collagens
elastase(s)
atherosclerosis
hypertension

Authors

Wojciech Wojakowski
Jan Gmiński 9

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail: viamedica@viamedica.pl