caa a22 4500 477072585 CHVBK 20180405111430.0 cr unu---uuuuu 170330e19961101xx s 000 0 eng 10.1007/BF00051002 doi (NATIONALLICENCE)springer-10.1007/BF00051002 Effect of prolonged inhibition of neutral endopeptidase on cardiac hypertrophy in rats with myocardial infarction [Elektronische Daten] [C. Marie, C. Mossiat, C. Gros, T. Monteil, J. Bralet] Summary: Myocardial infarction was induced in rats by ligation of the left coronary artery. Treatment with TM1, a prodrug of SQ 28,603, an inhibitor of neutral endopeptidase (NEP, EC 3.4.24.11), was started 18-20 hours after ligation and was continued for 4 weeks (100 mg/kg, orally, twice daily). Morphological and biochemical parameters were assessed at the end of therapy. The treatment resulted in a significant reduction of heart hypertrophy, which was restricted to the parts of myocardium hemodynamically upstream of the infarcted left ventricle. The weights of the right ventricle and atria were reduced by 15-20%, whereas the treatment had no effect on the left ventricle and septum weights. Treatment led to an almost complete inhibition of plasma NEP activity and to a slight decrease (-14%, p<0.05) in plasma ACE activity. Plasma ANF level increased 3.8-fold after ligation, and treatment resulted in a slight (+29%) and nonsignificant additional increase in the ANF level. The amount of hydroxyproline in the right ventricle was enhanced by +207% in control ligated rats and by +140% (NS) in treated rats. These data indicate that prolonged NEP inhibition exerts a favorable effect in heart failure by reducing the development of right ventricular and atrial hypertrophy. These effects may result from an improvement in hemodynamic conditions, leading to a reduction in cardiac preload. Kluwer Academic Publishers, 1996 neutral endopeptidase nationallicence TM1 nationallicence heart failure nationallicence cardiac hypertrophy nationallicence atrial natriuretic factor nationallicence Marie C. Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France aut Mossiat C. Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France aut Gros C. Unité de Neurobiologie et Pharmacologie (U 109) de l'INSERM, Centre Paul Broca, Paris, France aut Monteil T. Laboratoire de Chimie organique (URA CNRS 464 et IRCOF), Université de Rouen, France aut Bralet J. Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France aut Cardiovascular Drugs and Therapy Kluwer Academic Publishers 10/5(1996-11-01), 593-598 0920-3206 10:5<593 1996 10 10557 https://doi.org/10.1007/BF00051002 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00051002 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Marie C. Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France aut NATIONALLICENCE 700 1- Mossiat C. Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France aut NATIONALLICENCE 700 1- Gros C. Unité de Neurobiologie et Pharmacologie (U 109) de l'INSERM, Centre Paul Broca, Paris, France aut NATIONALLICENCE 700 1- Monteil T. Laboratoire de Chimie organique (URA CNRS 464 et IRCOF), Université de Rouen, France aut NATIONALLICENCE 700 1- Bralet J. Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France aut NATIONALLICENCE 773 0- Cardiovascular Drugs and Therapy Kluwer Academic Publishers 10/5(1996-11-01), 593-598 0920-3206 10:5<593 1996 10 10557 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer