Korean Circ J.
2005 Sep;35(9):665-671. 10.4070/kcj.2005.35.9.665.
Bosentan Attenuates Compensatory Left Ventricular Hypertrophy Induced by Aortocaval Fistula in Rats
- Affiliations
-
- 1Department of Pediatrics, College of Medicine, Dongguk University, Gyeongju, Korea. lds117@dongguk.ac.kr
- 2Department of Physiology, College of Medicine, Dongguk University, Gyeongju, Korea.
- 3Department of Anatomy, College of Medicine, Dongguk University, Gyeongju, Korea.
- KMID: 1859019
- DOI: http://doi.org/10.4070/kcj.2005.35.9.665
Abstract
- BACKGROUND AND OBJECTIVES
Endothelin-1 (ET-1) is increased in advanced congestive heart failure and pulmonary hypertension associated with increased pulmonary blood flow. The role of ET-1 and the protective effect of the dual endothelin receptor antagonist, Bosentan, were investigated in overcirculation-induced compensatory left ventricular (LV) hypertrophy using aortocaval fistula (AVF) rats.
MATERIALS AND METHODS
Twenty one 8-week-old rats were randomized into sham control, AVF and Bosentan (100 mg/kg/day) treatment groups. Four weeks later, the cardiac hypertrophy, pulmonary artery morphometry, plasma and tissue levels of ET-1 and the immunoreactive signal of ET-1 were evaluated in the heart and lung tissues.
RESULTS
Chronic AVF developed LV hypertrophy and markedly increased the plasma and tissue ET-1 levels in the heart and lung compared to those in the controls (p<0.05), and these changes were attenuated by Bosentan treatment (p<0.05). However, the wall thickness of the pulmonary arteriole did not change. In addition, the immunoreactive signal of ET-1 was increased in the heart after AVF compared with the controls, and was also slightly decreased with Bosentan treatment. However, there were no remarkable differences in the lung tissue.
CONCLUSION
ET-1 was up-regulated in compensatory LV hypertrophy induced by AVF. Bosentan attenuates cardiac hypertrophy and decreases the ET-1 levels in the plasma, heart and lung. Therefore, it is speculate that chronic treatment of an ET-1 antagonist may provide an additional strategy for AVF-induced compensatory LV hypertrophy.
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