Effect of losartan on sarcoplasmic reticulum Ca2+ handing proteins in heart failure rabbit.
- Author:
Yan YAO
1
;
Cong-xin HUANG
;
Gao CHEN
;
Lin XU
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II Type 1 Receptor Blockers; pharmacology; Animals; Calcium; metabolism; Calcium Channels; drug effects; Calmodulin; biosynthesis; genetics; Female; Heart Failure; drug therapy; metabolism; Losartan; pharmacology; Male; Rabbits; Ryanodine Receptor Calcium Release Channel; biosynthesis; Sarcoplasmic Reticulum; drug effects; metabolism
- From: Chinese Journal of Cardiology 2006;34(9):793-796
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of losartan on mRNA expression of myocardial sarcoplasmic reticulum calcium handling proteins (SERCA2, RyR2 and PLB) and the role of which in prevention of chronic heart failure in rabbit.
METHODSAfter chronic heart failure was induced by ligation of the left anterior descending artery in rabbits, the animals were treated with losartan. At 8 weeks after ligation, left ventricular function, hemodynamic parameters, and SERCA2, RyR2, PLB mRNA expressions were observed.
RESULTSCompared with the control group (group C), LVEDP in the infarcted group (group I) increased (P < 0.01), while +dp/dt(max) and -dp/dt(max) decreased significantly (P < 0.01). LVEDP was lower but +dp/dt(max) and -dp/dt(max) significantly higher in the losartan treated group (group L) than those in group I (P < 0.05). SERCA2, RyR2, and PLB mRNA expressions in group I were remarkably lower than those in group L (P < 0.01) and group C (P < 0.01), respectively.
CONCLUSIONLosartan can improve cardiac function, probably owing to its upregulating mRNA expressions of myocardial sarcoplasmic reticulum Ca(2+) handling proteins (RyR2, SERCA2 and PLB) in the prevention of heart failure.