Document Detail


Effect of pressure overload and its recovery on the rat carotid artery: change of vascular reactivity and remodeling process.
MedLine Citation:
PMID:  16440149     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Compared to chronic hypertension, little is known about the pathophysiology of acute hypertension and its recovery. To characterize this, we investigated the functional and structural properties of the common carotid arteries (CCA) from 35 rats. We established a unilateral and reversible carotid arterial hypertension model using the partial transverse aortic constriction (TAC) technique. By TAC, the right CCAs were made to endure a pressure-overload environment, while the left CCAs remained under normotension. The TACs were removed 2 weeks later, which unloaded the hypertensive effects. We compared the contractile, histological, and molecular responses of the CCA before TAC, during TAC (the hypertension period), and after removal of TAC (the recovery period). Vessel contractility was nearly abolished during 2 weeks of TAC. The recovery process from hypertension showed an initial hypercontractile period within a week. The relaxation response due to acetylcholine, as measured during the recovery period, showed a longer time course than the contractility for recovering its magnitude. During the hypertension period, the media thickness increased and this persisted throughout the recovery period. Apoptosis of the endothelial layer was significantly increased during the hypertension period and this disappeared 2 weeks after recovery. Expression of endothelial NO synthase was not detectable at the end of the hypertension period, but this gradually returned to the basal level after 2 weeks of recovery. Although increased contractility is usually expected in chronic hypertensive vessels, an abrupt pressure overload decreases contractility and the endothelium-dependent relaxation. It also increases endothelial apoptosis and the media thickness. These findings have clinical relevance, and they could be applied to human acute and severe hypertension and its recovery.
Authors:
Jin-Sook Kwon; Sang-Jin Lee; Young-Gyu Kim; Jang-Whan Bae; Kyung-Kuk Hwang; Myeong-Chan Cho; Dong-Woon Kim
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Heart and vessels     Volume:  21     ISSN:  0910-8327     ISO Abbreviation:  Heart Vessels     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2006-01-27     Completed Date:  2007-08-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8511258     Medline TA:  Heart Vessels     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  48-55     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Chungbuk National University Hospital, 62 Gaeshin-Dong, Heungduk-Gu, Cheongju, South Korea.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Animals
Apoptosis
Blood Pressure* / drug effects
Blotting, Western
Carotid Artery, Common / enzymology,  pathology*,  physiopathology*
Disease Models, Animal
Endothelium, Vascular / enzymology,  pathology,  physiopathology
Hypertension / enzymology,  pathology*,  physiopathology*
Immunohistochemistry
Male
Nitric Oxide Synthase Type III / biosynthesis
Potassium Chloride / pharmacology
Rats
Rats, Sprague-Dawley
Recovery of Function* / drug effects
Serotonin Agents / pharmacology
Time Factors
Tunica Media / pathology,  physiopathology
Vascular Resistance / drug effects
Vasoconstriction / drug effects
Vasodilation / drug effects
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Serotonin Agents; 0/Vasodilator Agents; 51-84-3/Acetylcholine; 7447-40-7/Potassium Chloride; EC 1.14.13.39/Nitric Oxide Synthase Type III

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


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