Effects of Losartan and Amlodipine on Left Ventricular Remodeling and Function in Young Stroke-Prone Spontaneously Hypertensive Rats
Background: The purpose of this study was to evaluate the effects of prehypertensive losartan and amlodipine administration on left ventricular (LV) remodeling and function in spontaneously hypertensive rats-stroke prone (SHRSP). Methods: Spontaneously hypertensive rats-stroke prone were prehyperten...
Saved in:
Published in | Acta Cardiologica Sinica Vol. 30; no. 4; pp. 316 - 324 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English Chinese |
Published |
台灣
中華民國心臟學會
01.07.2014
Taiwan Society of Cardiology |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Background: The purpose of this study was to evaluate the effects of prehypertensive losartan and amlodipine administration on left ventricular (LV) remodeling and function in spontaneously hypertensive rats-stroke prone (SHRSP). Methods: Spontaneously hypertensive rats-stroke prone were prehypertensively administered losartan, amlodipine, or vehicle.Wistar-Kyoto ratswere used as a control. Blood pressure of the ratswas determined by tail-cuffmethod, and LV structure and function were measured by echocardiography and LV cannulation. Collagen volume fraction was analyzed by picrosirius red staining. Protein expressions of brain natriuretic peptide (BNP) and angiotensin II type 1 (AT1R) and type 2 (AT2R) receptors were determined by use of theWestern blotting method. Results: Although both drugs downregulated BNP protein expression, the LV remodeling and function were more improved with losartan than with amlodipine treatment. Losartan upregulated AT1R and downregulated AT2R protein expression. Conclusions: Both drugs inhibited LV remodeling and improved LV function in prehypertensively treated SHRSP. Losartan provided better continued heart protection, potentially due to its persistent inhibition of AT1R and activation of AT2R in the myocardium. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1011-6842 |