Effects of Pressure Overload and its Recovery on Vascular Reactivity and Remodeling of the Rat Carotid Artery.
10.4070/kcj.2003.33.10.936
- Author:
Jin Sook KWON
1
;
Sang Jin LEE
;
Young Gyu KIM
;
Young Chul KIM
;
Ki Seok KIM
;
Kyung Kuk HWANG
;
Tae Jin YOUN
;
Myeong Chan CHO
;
Dong Woon KIM
Author Information
1. Department of Internal Medicine, Chungbuk National University, Cheongju, Korea. kdwoon@chungbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Hypertension;
Arteries;
Contractility;
Remodeling;
Nitric oxide
- MeSH:
Acetylcholine;
Adventitia;
Animals;
Apoptosis;
Arteries;
Carotid Arteries*;
Carotid Artery, Common;
Constriction;
Hypertension;
Ligation;
Nitric Oxide;
Rats*;
Relaxation
- From:Korean Circulation Journal
2003;33(10):936-948
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: The Vascular system exhibits altered morphological and functional properties during hypertension and after anti-hypertensive therapy. To characterize such changes, the contractile, histological and molecular responses in the common carotid arteries (CCA) were compared in 35 rats. MATERIALS AND METHODS: By partial transverse aortic constriction (TAC), the right CCAs were made to lie under a high pressure environment, while the left CCAs remained under normotension, the latter being used as control vessels. The ligations were removed after two weeks, to enable the recovery process to begin. RESULTS: The vessel contractility, two weeks after the TAC, was nearly abolished. The recovery process from high pressure showed an initial hypercontractile period of around 1-2 week after recovery, prior to the subsequent decline to a normal contractility after 2 weeks. The relaxation response due to acetylcholine was minimal at the end of the hypertensive period, recovered slowly, and reached a normal magnitude after 4 weeks. A high pressure increases the medial thickness & area, and enhances the adventitial tissue formation. These changes persist during the first 4 weeks of recovery, after which normotension returns. Apoptosis at the endothelial layer was significantly increased two weeks after the TAC, but normalized two weeks after recovery. The expression of ecNOS was not detect 2 weeks after the TAC, but gradually returned to a basal level at 2 weeks after the untying. CONCLUSION: A high blood pressure causes decreases in the contractility and endothelium-dependent relaxation. It also increases endothelial apoptosis, the medial thickness & area, and enhances the adventitial tissue formation. The recovery processes from high blood pressure are not uniform, but show different normalizations among the structural, contractile and apoptotic parameters.
