| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
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| Research Abstract |
OBJECTIVES : Myosin and collagen are major components of the heart. In has been revealed that when the heart receives pressure overload, not only contractile proteins but also collagen metabolisms change quantitatively and qualitatively. However, relative changes in contractile and non-contractile protein metabolisms in cardiac hypertrophy are not clarified simultaneously, and its meaning remains unclear. Moreover, beta-receptors, which are closely related to cardiac function, are known to change during the development of cardiac hypertrophy. In this study, we examined the above-mentioned parameters of pressure-overloaded and nonpressure-overloaded ventricles simultaneously. We also examined the effects of antihypertenive drugs on the above-mentioned parameters of hypertrophied heart and analyzed merits and demerits of these antihypertensive agents from the view points of contractile and noncontractile protein metabolisms. MATERIALS & METHODS : Monocrotaline-induced right ventricular h
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ypertrophy(RVH)model in rat was u ed. Changes in myosin isoenzymes, and qualitative and quantitative changes in collagen in the ventricles were examined. Changes in beta-receptors were also examined. Moreover, effects of ACE inhibitor and Ca antagonist on protein metabolisms of RVH were also examined. RESULTS : (1)MIE in the RV as well as in the LV shifted from Vl to V3 during the development of RVH. (2)Although collagen concentration of the ventricles did not alter, types Ill and V collagens in the RV increased. (3)Numbers of beta-receptors decreased not only in the RV, but also in the LV. These changes became much more prominent as RVH became pronounced, resulting in congestive heart failure. (4)Derapril-HCl(ACE inhibitor ; 30 mg/kg/day)and Nilvadipine(Ca antagonist ; 3 mg/kg/day)reduced systolic RV pressure to the same extent and inhibited RVH. The inhibitory effect of ACE inhibitor was more strong than that of Ca antagonist. Both drugs reversed the changes in MIE to the same extent. Although total collagen contents of the RV decreased by treatment with both drugs, ACE inhibitor did not decrease collagen concentration while Ca antagonist decreased collagen concentration. Moreover, ACE inhibitor did not reverse changes in collagen types while Ca antagonist reversed them. CONCLUSIONS : Our results revealed that the heart adapts to pressure overload by changing contractile and noncontractile protein metabolisms quantitatively and qualitatively. However, pronounced changes in these protein metabolisms lead to maladaptation to a pressure overload. Detailed effects of anti-hypertensive drugs on contractile and noncontractile protein metabolisms, but not simple effects of them on cardiac mass, are necessary to evaluate the exact usefulness of anti-hypertensive agents on cardiac hypertrophy in response to a pressure overload. Less
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