View : 23 Download: 0
Changes of gene expressions in spontaneously hypertensive rat model after losartan treatment
- Changes of gene expressions in spontaneously hypertensive rat model after losartan treatment
- Cha J.H.; Lee H.R.; Kim K.C.; Cho M.-S.; Hong Y.M.
- Ewha Authors
- 홍영미; 조민선; 김관창
- SCOPUS Author ID
- 홍영미; 조민선; 김관창
- Issue Date
- Journal Title
- Korean Circulation Journal
- vol. 42, no. 11, pp. 761 - 768
- SCIE; SCOPUS; KCI
- Background and Objectives: The renin angiotensin system seems to play an important role in the development of cardiac and vascular hypertrophy in hypertension. The changes in pathology, and gene expressions of the angiotensin II receptor type 1A (AT1A) and angiotensin converting enzyme (ACE) were investigated in order to explore the effects of losartan in spontaneously hypertensive rat (SHR) models. Materials and Methods: Twelve week-old male Wistar rats were grouped as follows: control (C) group, hypertension (H) group, and losartan (L) group in which SHR was treated with losartan (10 mg/kg/day). Western blot and reverse transcription-polymerase chain reaction analysis regarding seven genes such as endothelin-1, ACE, AT1A, neutrophil cytosolic factor, brain natriuretic peptide, troponin I, endothelial nitric oxide synthase were performed. Results: Systolic blood pressure was significantly decreased in the L group compared with the H group in weeks 3 and 5. ACE and AT1A proteins in the L group were lower than H group in week 5. Conclusion: Losartan reduced blood pressure, cardiac hypertrophy and protein expressions of ACE and AT1A. Changes of protein expressions were more sensitive than changes in pathology. Further study is needed for the differing doses of losartan in SHR models. Copyright © 2012 The Korean Society of Cardiology.
- Appears in Collections:
- 의학전문대학원 > 의학과 > Journal papers
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.