Document Detail


Associations between collagen synthesis and degradation and aortic function in arterial hypertension.
MedLine Citation:
PMID:  20134406     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Studies have suggested that collagen accumulation in the aortic wall may contribute to the stiff aorta in arterial hypertension. However, data in human hypertension are limited. In this investigation, relations between markers of collagen metabolism and aortic function in patients with arterial hypertension were evaluated.
METHODS: We studied 72 hypertensive patients (age 53 +/- 5 years) and 27 age- and gender-matched normotensive individuals. Elastic properties of the aorta were assessed by aortic pulse wave velocity (carotid-to-femoral pulse wave velocity (PWVc-f)). Free amino-terminal propeptides of precollagen type I (PINP, reflecting collagen I synthesis), serum telopeptides of collagen type I (CITP, an index of collagen I degradation), free amino-terminal propeptides on precollagen type III (PIIINP, reflecting collagen III metabolism), prometalloproteinase-1 (proMMP-1), and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels were determined by commercially available immunoassays.
RESULTS: Patients with arterial hypertension had greater PWVc-f (P = 0.01); and higher levels of PINP/CITP compared to control (P = 0.04). PWVc-f was significantly associated with PINP/CITP ratio (analysis of variance (ANOVA), P = 0.03). Hypertensive patients had significantly higher levels of proMMP-1/TIMP-1 (P = 0.04); PWVc-f was significantly associated with proMMP-1 (ANOVA, P = 0.03) and proMMP-1/TIMP-1 (ANOVA, P = 0.04). Associations between PWVc-f and proMMP-1 and between PWVc-f and PINP/CITP ratio remained significant after adjustment for PWVc-f confounders and antihypertensive treatment.
CONCLUSIONS: Alterations in collagen turnover that favor collagen type I synthesis; as well as proMMP-1 expression are related to increased aortic stiffness in treated hypertensive individuals without left ventricular (LV) hypertrophy.
Authors:
Dimitrios A Stakos; Dimitrios N Tziakas; George K Chalikias; Kostantina Mitrousi; Christina Tsigalou; Harisios Boudoulas
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Publication Detail:
Type:  Journal Article     Date:  2010-02-04
Journal Detail:
Title:  American journal of hypertension     Volume:  23     ISSN:  1941-7225     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-20     Completed Date:  2010-07-22     Revised Date:  2011-06-30    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  United States    
Other Details:
Languages:  eng     Pagination:  488-94     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece. dstakos@med.duth.gr
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MeSH Terms
Descriptor/Qualifier:
Aorta / physiopathology*
Case-Control Studies
Collagen / metabolism*
Collagen Type I / metabolism
Elasticity / physiology
Female
Humans
Hypertension / physiopathology*
Male
Matrix Metalloproteinase 1 / metabolism
Middle Aged
Peptide Fragments / metabolism
Procollagen / metabolism
Regional Blood Flow / physiology
Tissue Inhibitor of Metalloproteinase-1 / metabolism
Chemical
Reg. No./Substance:
0/Collagen Type I; 0/Peptide Fragments; 0/Procollagen; 0/Tissue Inhibitor of Metalloproteinase-1; 0/procollagen Type I N-terminal peptide; 0/procollagen Type III-N-terminal peptide; 9007-34-5/Collagen; EC 3.4.24.7/Matrix Metalloproteinase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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