Pressure overload induces cardiac hypertrophy in angiotensin II type 1A receptor knockout mice
Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy. Moreover, it has been reported that pressure overload-induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the...
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Published in | Circulation (New York, N.Y.) Vol. 97; no. 19; pp. 1952 - 1959 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hagerstown, MD
Lippincott Williams & Wilkins
19.05.1998
American Heart Association, Inc |
Subjects | |
Online Access | Get full text |
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Abstract | Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy. Moreover, it has been reported that pressure overload-induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT1) in vitro. These results suggest that the AT1-mediated signaling is critical for the development of mechanical stress-induced cardiac hypertrophy.
To determine whether AT1-mediated signaling is indispensable for the development of pressure overload-induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT1A knockout (KO) mice. Quantitative reverse transcriptase-polymerase chain reaction revealed that the cardiac AT1 (probably AT1B) mRNA levels in AT1A KO mice were <10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis.
AT1-mediated Ang II signaling is not essential for the development of pressure overload-induced cardiac hypertrophy. |
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AbstractList | Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy. Moreover, it has been reported that pressure overload-induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT1) in vitro. These results suggest that the AT1-mediated signaling is critical for the development of mechanical stress-induced cardiac hypertrophy.
To determine whether AT1-mediated signaling is indispensable for the development of pressure overload-induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT1A knockout (KO) mice. Quantitative reverse transcriptase-polymerase chain reaction revealed that the cardiac AT1 (probably AT1B) mRNA levels in AT1A KO mice were <10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis.
AT1-mediated Ang II signaling is not essential for the development of pressure overload-induced cardiac hypertrophy. BACKGROUND: Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy. Moreover, it has been reported that pressure overload-induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT1) in vitro. These results suggest that the AT1-mediated signaling is critical for the development of mechanical stress-induced cardiac hypertrophy. METHODS AND RESULTS: To determine whether AT1-mediated signaling is indispensable for the development of pressure overload-induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT1A knockout (KO) mice. Quantitative reverse transcriptase-polymerase chain reaction revealed that the cardiac AT1 (probably AT1B) mRNA levels in AT1A KO mice were 10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis. CONCLUSIONS: AT1-mediated Ang II signaling is not essential for the development of pressure overload-induced cardiac hypertrophy. BACKGROUNDMany studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy. Moreover, it has been reported that pressure overload-induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT1) in vitro. These results suggest that the AT1-mediated signaling is critical for the development of mechanical stress-induced cardiac hypertrophy.METHODS AND RESULTSTo determine whether AT1-mediated signaling is indispensable for the development of pressure overload-induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT1A knockout (KO) mice. Quantitative reverse transcriptase-polymerase chain reaction revealed that the cardiac AT1 (probably AT1B) mRNA levels in AT1A KO mice were <10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis.CONCLUSIONSAT1-mediated Ang II signaling is not essential for the development of pressure overload-induced cardiac hypertrophy. Background —Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload–induced cardiac hypertrophy. Moreover, it has been reported that pressure overload–induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT 1 ) in vitro. These results suggest that the AT 1 -mediated signaling is critical for the development of mechanical stress–induced cardiac hypertrophy. Methods and Results —To determine whether AT 1 -mediated signaling is indispensable for the development of pressure overload–induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT 1A knockout (KO) mice. Quantitative reverse transcriptase–polymerase chain reaction revealed that the cardiac AT 1 (probably AT 1B ) mRNA levels in AT 1A KO mice were <10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis. Conclusions —AT 1 -mediated Ang II signaling is not essential for the development of pressure overload–induced cardiac hypertrophy. |
Author | HARADA, K KOMURO, I MATSUBARA, H SUGAYA, T KUDOH, S KIJIMA, K YAZAKI, Y HAYASHI, D SHIOJIMA, I MIZUNO, T MURAKAMI, K |
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Keywords | Heart Pathogenesis Rodentia Cardiovascular disease Pathology Vertebrata Optical microscopy Mammalia Mouse Heart disease Animal Angiotensin II Hypertrophy Biological receptor |
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Snippet | Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy.... Background —Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload–induced cardiac... BACKGROUND: Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac... BACKGROUNDMany studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac... |
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SubjectTerms | Angiotensin II - pharmacology Animals Aorta, Abdominal - physiology Biological and medical sciences Blood Pressure - drug effects Cardiology. Vascular system Cardiomegaly - etiology Cardiomegaly - genetics Cardiomegaly - physiopathology Echocardiography Heart Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hypertension - complications Hypertension - physiopathology Medical sciences Mice Mice, Knockout Polymerase Chain Reaction Receptor, Angiotensin, Type 1 Receptors, Angiotensin - biosynthesis Receptors, Angiotensin - deficiency Receptors, Angiotensin - genetics Receptors, Angiotensin - physiology RNA, Messenger - biosynthesis Signal Transduction Transcription, Genetic |
Title | Pressure overload induces cardiac hypertrophy in angiotensin II type 1A receptor knockout mice |
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