Renin-Angiotensin-Aldosterone Signaling Inhibitors-Losartan, Enalapril, and Cardosten-Prevent Infarction-induced Heart Failure Development in Rats

Context • The activation of the renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of congestive heart failure, which is the reason that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin 2 receptor blockers (ARBs) have become established therapi...

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Elmentve itt :
Bibliográfiai részletek
Szerzők: Kiss Krisztina
Fekete Veronika
Pálóczi János
Sárközy Márta
Murlasits Zsolt
Pipis Judit
Kheyfets Irina A.
Dugina Julia L.
Sergeeva Svetlana A.
Epstein Oleg I.
Csonka Csaba
Csont Tamás Bálint
Ferdinandy Péter
Bencsik Péter
Dokumentumtípus: Cikk
Megjelent: 2016-03
Sorozat:Alternative therapies in health and medicine 22 No. 2
mtmt:3044918
Online Access:http://publicatio.bibl.u-szeged.hu/6585
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245 1 0 |a Renin-Angiotensin-Aldosterone Signaling Inhibitors-Losartan, Enalapril, and Cardosten-Prevent Infarction-induced Heart Failure Development in Rats  |h [elektronikus dokumentum] /  |c  Kiss Krisztina 
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520 3 |a Context • The activation of the renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of congestive heart failure, which is the reason that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin 2 receptor blockers (ARBs) have become established therapies for heart failure. However, it is still not known whether preventive treatment with losartan or enalapril can reduce symptoms of infarction-induced heart failure. Ultra-low dose (ULD) drug therapy is thought to exert specific activity, with a lower chance of side effects. Objectives • The research team had hypothesized that preventive treatment with inhibitors of RAAS signaling-losartan, enalapril, and a preparation of a ULD antibody (ie, cardosten), which target the angiotensin type 1 (AT1) receptor-might alleviate pathological hypertrophy and/or functional decline in infarction-induced heart failure. Methods • The research team treated male Wistar rats orally for 30 d with 20 mg/kg of losartan, 10 mg/kg enalapril, 5 or 7.5 mL/kg of cardosten, or a control solution, started 1 d prior to permanent coronary occlusion. A sham-operated group functioned as a second control group. Settings • The study was conducted at the Department of Biochemistry of the Faculty of Medicine at the University of Szeged in Szeged, Hungary, in cooperation with the Pharmahungary Group, also in Szeged, Hungary, and with OOO "NPF" Materia Medica Holding Ltd in Moscow, Russia. Outcome Measures • To determine cardiac functional parameters in vivo, the research team inserted a catheter into the left ventricle of the rats and measured the parameters of ventricular pressure, and cardiac output was determined by thermodilution. Morphological parameters were measured after heart isolation in transverse sections by a digital caliper. Results • A total of 30 d after permanent coronary ligation, both losartan and enalapril, significantly decreased mean arterial blood pressure (MABP), attenuated the development of the left-ventricular anterior-wall and septum hypertrophy, and reduced scar thickness compared with the vehicle control group. The deterioration of cardiac output and the increase in total peripheral resistance (TPR) due to coronary ligation were significantly inhibited by both losartan and enalapril. The effects of cardosten were comparable with those of losartan and enalapril on cardiac morphology, left ventricular function, and TPR; however, it did not influence MABP. Moreover, in contrast to losartan and enalapril, cardosten did not decrease the rate of survival. Conclusions • The study was the first to have demonstrated that preventive treatment with losartan, enalapril, or cardosten can attenuate pathological hypertrophy in infarction-induced heart failure in rats. 
700 0 1 |a Fekete Veronika  |e aut 
700 0 1 |a Pálóczi János  |e aut 
700 0 1 |a Sárközy Márta  |e aut 
700 0 1 |a Murlasits Zsolt  |e aut 
700 0 1 |a Pipis Judit  |e aut 
700 0 1 |a Kheyfets Irina A.  |e aut 
700 0 1 |a Dugina Julia L.  |e aut 
700 0 1 |a Sergeeva Svetlana A.  |e aut 
700 0 1 |a Epstein Oleg I.  |e aut 
700 0 1 |a Csonka Csaba  |e aut 
700 0 1 |a Csont Tamás Bálint  |e aut 
700 0 1 |a Ferdinandy Péter  |e aut 
700 0 1 |a Bencsik Péter  |e aut 
856 4 0 |u http://publicatio.bibl.u-szeged.hu/6585/2/3044918%20.pdf  |z Dokumentum-elérés