Captopril and losartan improved myocardial function and prevented subcellular remodeling and gene expression changes in rats with pressure overload-induced cardiac hypertrophy.
Does captopril or losartan improve myocardial function and prevent subcellular remodeling in rats with pressure overload-induced cardiac hypertrophy?
Captopril and losartan improve myocardial function in pressure overload-induced cardiac hypertrophy by preventing changes in gene expression and subcellular remodeling.
In view of the activation of renin-angiotensin system under conditions associated with pressure overload on the heart, we examined the effects of captopril, an angiotensin converting enzyme inhibitor, and losartan, an angiotensin II receptor antagonist, on cardiac function, myofibrillar ATPase and sarcoplasmic reticular (SR) Ca2+-pump (SERCA2) activities, as well as myosin and SERCA2 gene expression in hypertrophied hearts. Cardiac hypertrophy was induced in rats treated with or without captopril or losartan by banding the abdominal aorta for 8 weeks; sham operated animals served as control. Decrease in left ventricular developed pressure, +dP/dt and -dP/dt as well as increase in left ventricular end diastolic pressure and increased muscle mass due to pressure overload were prevented by captopril or losartan. Treatment of animals with captopril or losartan also attenuated the pressure overload-induced depression in myofibrillar Ca2+-stimulated ATPase, myosin ATPase, SR Ca2+-uptake and SR Ca2+-release activities. An increase in beta-myosin heavy chain mRNA and a decrease in alpha-myosin heavy chain mRNA as well as depressed SERCA2 protein and SERCA2 mRNA levels were prevented by captopril or losartan. These results suggest that both captopril and losartan improve myocardial function in cardiac hypertrophy by preventing changes in gene expression and subsequent subcellular remodeling due to pressure overload.
Liu et al. (Fri,) conducted a other in Cardiac hypertrophy. Captopril or losartan vs. Untreated pressure overload and sham-operated controls was evaluated on Cardiac function, myofibrillar ATPase and SERCA2 activities, and gene expression. Captopril and losartan improved myocardial function and prevented subcellular remodeling and gene expression changes in rats with pressure overload-induced cardiac hypertrophy.