Renin Inhibition Improves Cardiac Function and Remodeling After Myocardial Infarction Independent of Blood Pressure
Pharmacological renin inhibition with aliskiren is an effective antihypertensive drug treatment, but it is currently unknown whether aliskiren is able to attenuate cardiac failure independent of its blood pressure–lowering effects. We investigated the effect of aliskiren on cardiac remodeling, apopt...
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Published in | Hypertension (Dallas, Tex. 1979) Vol. 52; no. 6; pp. 1068 - 1075 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
American Heart Association, Inc
01.12.2008
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Abstract | Pharmacological renin inhibition with aliskiren is an effective antihypertensive drug treatment, but it is currently unknown whether aliskiren is able to attenuate cardiac failure independent of its blood pressure–lowering effects. We investigated the effect of aliskiren on cardiac remodeling, apoptosis, and left ventricular (LV) function after experimental myocardial infarction (MI). C57J/bl6 mice were subjected to coronary artery ligation and were treated for 10 days with vehicle or aliskiren (50 mg/kg per day via an SC osmopump), whereas sham-operated animals served as controls. This dose of aliskiren, which did not affect systemic blood pressure, improved systolic and diastolic LV function, as measured by the assessment of pressure-volume loops after MI. Furthermore, after MI LV dilatation, cardiac hypertrophy and lung weights were decreased in mice treated with aliskiren compared with placebo-treated mice after MI. This was associated with a normalization of the mitogen-activated protein kinase P38 and extracellular signal-regulated kinases 1/2, AKT, and the apoptotic markers bax and bcl-2 (all measured by Western blots), as well as the number of TUNEL-positive cells in histology. LV dilatation, as well as the associated upregulation of gene expression (mRNA abundance) and activity (by zymography) of the cardiac metalloproteinase 9 in the placebo group after MI, was also attenuated in the aliskiren-treated group. Aliskiren improved LV dysfunction after MI in a dose that did not affect blood pressure. This was associated with the amelioration of cardiac remodelling, hypertrophy, and apoptosis. |
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AbstractList | Pharmacological renin inhibition with aliskiren is an effective antihypertensive drug treatment, but it is currently unknown whether aliskiren is able to attenuate cardiac failure independent of its blood pressure–lowering effects. We investigated the effect of aliskiren on cardiac remodeling, apoptosis, and left ventricular (LV) function after experimental myocardial infarction (MI). C57J/bl6 mice were subjected to coronary artery ligation and were treated for 10 days with vehicle or aliskiren (50 mg/kg per day via an SC osmopump), whereas sham-operated animals served as controls. This dose of aliskiren, which did not affect systemic blood pressure, improved systolic and diastolic LV function, as measured by the assessment of pressure-volume loops after MI. Furthermore, after MI LV dilatation, cardiac hypertrophy and lung weights were decreased in mice treated with aliskiren compared with placebo-treated mice after MI. This was associated with a normalization of the mitogen-activated protein kinase P38 and extracellular signal-regulated kinases 1/2, AKT, and the apoptotic markers bax and bcl-2 (all measured by Western blots), as well as the number of TUNEL-positive cells in histology. LV dilatation, as well as the associated upregulation of gene expression (mRNA abundance) and activity (by zymography) of the cardiac metalloproteinase 9 in the placebo group after MI, was also attenuated in the aliskiren-treated group. Aliskiren improved LV dysfunction after MI in a dose that did not affect blood pressure. This was associated with the amelioration of cardiac remodelling, hypertrophy, and apoptosis. |
Author | Lettau, Olga Savvatis, Konstantinos Danser, A H. Jan Roks, Anton Riad, Alexander Becher, Peter Moritz Tschöpe, Carsten Schultheiss, Heinz-Peter Escher, Felicitas Westermann, Dirk |
AuthorAffiliation | From the Department of Cardiology and Pneumology (D.W., A.R., O.L., K.S., P.M.B., F.E., H.-P.S., C.T.), Campus Benjamin Franklin, Charité–Universitätsmedizin Berlin, Berlin, Germany; and the Division of Vascular Pharmacology and Metabolism (A.R., A.H.J.D.), Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands |
AuthorAffiliation_xml | – name: From the Department of Cardiology and Pneumology (D.W., A.R., O.L., K.S., P.M.B., F.E., H.-P.S., C.T.), Campus Benjamin Franklin, Charité–Universitätsmedizin Berlin, Berlin, Germany; and the Division of Vascular Pharmacology and Metabolism (A.R., A.H.J.D.), Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands |
Author_xml | – sequence: 1 givenname: Dirk surname: Westermann fullname: Westermann, Dirk organization: From the Department of Cardiology and Pneumology (D.W., A.R., O.L., K.S., P.M.B., F.E., H.-P.S., C.T.), Campus Benjamin Franklin, Charité–Universitätsmedizin Berlin, Berlin, Germany; and the Division of Vascular Pharmacology and Metabolism (A.R., A.H.J.D.), Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands – sequence: 2 givenname: Alexander surname: Riad fullname: Riad, Alexander – sequence: 3 givenname: Olga surname: Lettau fullname: Lettau, Olga – sequence: 4 givenname: Anton surname: Roks fullname: Roks, Anton – sequence: 5 givenname: Konstantinos surname: Savvatis fullname: Savvatis, Konstantinos – sequence: 6 givenname: Peter surname: Becher middlename: Moritz fullname: Becher, Peter Moritz – sequence: 7 givenname: Felicitas surname: Escher fullname: Escher, Felicitas – sequence: 8 givenname: A surname: Danser middlename: H. Jan fullname: Danser, A H. Jan – sequence: 9 givenname: Heinz-Peter surname: Schultheiss fullname: Schultheiss, Heinz-Peter – sequence: 10 givenname: Carsten surname: Tschöpe fullname: Tschöpe, Carsten |
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SubjectTerms | Amides - pharmacology Animals Antihypertensive Agents - pharmacology Apoptosis - drug effects Blood Pressure - drug effects Cardiomegaly - complications Cardiomegaly - drug therapy Cardiomegaly - pathology Collagen - genetics Collagen - metabolism Extracellular Matrix - enzymology Fumarates - pharmacology Hypertension, Renal - complications Hypertension, Renal - drug therapy Male Matrix Metalloproteinase 9 - genetics Matrix Metalloproteinase 9 - metabolism Mice Mice, Inbred C57BL Myocardial Infarction - complications Myocardial Infarction - drug therapy Myocardial Infarction - pathology Myocardium - metabolism Renin - antagonists & inhibitors Renin - metabolism RNA, Messenger - metabolism Tissue Inhibitor of Metalloproteinase-1 - genetics Tissue Inhibitor of Metalloproteinase-1 - metabolism Ventricular Function, Left - drug effects Ventricular Remodeling - drug effects |
Title | Renin Inhibition Improves Cardiac Function and Remodeling After Myocardial Infarction Independent of Blood Pressure |
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