caa a22 4500 477119816 CHVBK 20180405111633.0 cr unu---uuuuu 170330e19960301xx s 000 0 eng 10.1007/BF00714327 doi (NATIONALLICENCE)springer-10.1007/BF00714327 Role of cardiac renin-angiotensin system in the development of pressure-overload left ventricular hypertrophy in rats with abdominal aortic constriction [Elektronische Daten] [Doodipala Reddy, Manjeet Singh, Sujata Ghosh, N. Ganguly] Possible involvement of cardiac renin-angiotensin system (RAS) in pressure overload induced left ventricular hypertrophy (LVH) was investigated. Rats were subjected to abdominal aortic constriction (AAC) and examined the effects of 4 weeks treatments with an angiotensin converting enzyme (ACE) inhibitor, captopril and a vasodilator, hydralazine on haemodynamics and ventricular RNA, DNA, protein and myosin isoform pattern in sham and hypertrophied rats. AAC increased the mean arterial pressure (MAP) and systolic blood pressure (SBP), and resulted in increased left ventricle/body weight ratio, LV thickness, RNA and protein content, however total DNA was not changed. The expression of fetal isogene, β-myosin heavy chain (β-MHC), was markedly enhanced where as u.-MHC was reduced. High-dose captopril (100 mg/kg p.o.,) significantly prevented the increase in haemodynamics, development of LVH, LV remodeling, increase in total protein, RNA and antithetical expression of myosin isoforms. Hydralazine (15 mg/kg p.o.,), did not modulate hypertrophic changes and low-dose captopril (1.5 mg/kg p.o.,) which has not produced any marked fall in MAP and SBP also modulated favourably the development of LVH and its biochemical markers. Thus, the prevention of the development of LVH and induction of β-MHC by non-hypotensive doses of captopril may be related to the blockade of intracardiac production of angiotensin II rather than circulating system. These results suggest that cardiac RAS may play an important role in pressure overload induced LVH. Kluwer Academic Publishers, 1996 angiotensin-II nationallicence captopril nationallicence left ventricular hypertrophy nationallicence myosin isoforms nationallicence hydralazine nationallicence Reddy Doodipala Department of Pharmacology, University Institute of Pharmaceutical Sciences, Panjab University, 160 014, Chandigarh, India aut Singh Manjeet Department of Pharmacology, University Institute of Pharmaceutical Sciences, Panjab University, 160 014, Chandigarh, India aut Ghosh Sujata Department of Experimental Medicine, Post Graduate Institute of Medical Education and Research, 160 012, Chandigarh, India aut Ganguly N. Department of Experimental Medicine, Post Graduate Institute of Medical Education and Research, 160 012, Chandigarh, India aut Molecular and Cellular Biochemistry Kluwer Academic Publishers 155/1(1996-03-01), 1-11 0300-8177 155:1<1 1996 155 11010 https://doi.org/10.1007/BF00714327 text/html Onlinezugriff via DOI 1 article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00714327 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Reddy Doodipala Department of Pharmacology, University Institute of Pharmaceutical Sciences, Panjab University, 160 014, Chandigarh, India aut NATIONALLICENCE 700 1- Singh Manjeet Department of Pharmacology, University Institute of Pharmaceutical Sciences, Panjab University, 160 014, Chandigarh, India aut NATIONALLICENCE 700 1- Ghosh Sujata Department of Experimental Medicine, Post Graduate Institute of Medical Education and Research, 160 012, Chandigarh, India aut NATIONALLICENCE 700 1- Ganguly N. Department of Experimental Medicine, Post Graduate Institute of Medical Education and Research, 160 012, Chandigarh, India aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Kluwer Academic Publishers 155/1(1996-03-01), 1-11 0300-8177 155:1<1 1996 155 11010 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer