Angiotensin II type 2 receptor deficiency exacerbates heart failure and reduces survival after acute myocardial infarction in mice
Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT1) and type 2 (AT2) receptors are known to be present in the heart, comparatively little is known about the latter. We therefore examined the role pl...
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| Published in | Circulation (New York, N.Y.) Vol. 107; no. 19; pp. 2406 - 2408 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
20.05.2003
American Heart Association, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT1) and type 2 (AT2) receptors are known to be present in the heart, comparatively little is known about the latter. We therefore examined the role played by AT2 receptors in post-AMI heart failure.
In wild-type mice subjected to AMI by coronary artery ligation, AT2 receptor immunoreactivity is upregulated in the infarct and border areas. Among AT2 receptor-null (-/-) mice, the 7-day survival rate after AMI was significantly lower than among wild-type mice (43% versus 67%; P<0.05). All sham-operated animals of both genotypes survived through the study. Ventricular mRNA levels for brain natriuretic peptide were elevated in both genotypes 24 hours after coronary occlusion, with levels in AT2-/- significantly higher than in wild-type mice, as were their lung weights, and histological examination revealed marked pulmonary congestion in the AT2-/- mice. Cardiac function was significantly decreased in AT2-/- mice 2 days after AMI.
AT2 receptor deficiency exacerbates short-term death rates and heart failure after experimental AMI in mice. The AT2 receptor may thus exert a protective effect on the heart after AMI. |
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| AbstractList | Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT1) and type 2 (AT2) receptors are known to be present in the heart, comparatively little is known about the latter. We therefore examined the role played by AT2 receptors in post-AMI heart failure.
In wild-type mice subjected to AMI by coronary artery ligation, AT2 receptor immunoreactivity is upregulated in the infarct and border areas. Among AT2 receptor-null (-/-) mice, the 7-day survival rate after AMI was significantly lower than among wild-type mice (43% versus 67%; P<0.05). All sham-operated animals of both genotypes survived through the study. Ventricular mRNA levels for brain natriuretic peptide were elevated in both genotypes 24 hours after coronary occlusion, with levels in AT2-/- significantly higher than in wild-type mice, as were their lung weights, and histological examination revealed marked pulmonary congestion in the AT2-/- mice. Cardiac function was significantly decreased in AT2-/- mice 2 days after AMI.
AT2 receptor deficiency exacerbates short-term death rates and heart failure after experimental AMI in mice. The AT2 receptor may thus exert a protective effect on the heart after AMI. BACKGROUNDAngiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT1) and type 2 (AT2) receptors are known to be present in the heart, comparatively little is known about the latter. We therefore examined the role played by AT2 receptors in post-AMI heart failure.METHODS AND RESULTSIn wild-type mice subjected to AMI by coronary artery ligation, AT2 receptor immunoreactivity is upregulated in the infarct and border areas. Among AT2 receptor-null (-/-) mice, the 7-day survival rate after AMI was significantly lower than among wild-type mice (43% versus 67%; P<0.05). All sham-operated animals of both genotypes survived through the study. Ventricular mRNA levels for brain natriuretic peptide were elevated in both genotypes 24 hours after coronary occlusion, with levels in AT2-/- significantly higher than in wild-type mice, as were their lung weights, and histological examination revealed marked pulmonary congestion in the AT2-/- mice. Cardiac function was significantly decreased in AT2-/- mice 2 days after AMI.CONCLUSIONSAT2 receptor deficiency exacerbates short-term death rates and heart failure after experimental AMI in mice. The AT2 receptor may thus exert a protective effect on the heart after AMI. Background— Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT 1 ) and type 2 (AT 2 ) receptors are known to be present in the heart, comparatively little is known about the latter. We therefore examined the role played by AT 2 receptors in post-AMI heart failure. Methods and Results— In wild-type mice subjected to AMI by coronary artery ligation, AT 2 receptor immunoreactivity is upregulated in the infarct and border areas. Among AT 2 receptor-null (−/−) mice, the 7-day survival rate after AMI was significantly lower than among wild-type mice (43% versus 67%; P <0.05). All sham-operated animals of both genotypes survived through the study. Ventricular mRNA levels for brain natriuretic peptide were elevated in both genotypes 24 hours after coronary occlusion, with levels in AT 2 −/− significantly higher than in wild-type mice, as were their lung weights, and histological examination revealed marked pulmonary congestion in the AT 2 −/− mice. Cardiac function was significantly decreased in AT 2 −/− mice 2 days after AMI. Conclusions— AT 2 receptor deficiency exacerbates short-term death rates and heart failure after experimental AMI in mice. The AT 2 receptor may thus exert a protective effect on the heart after AMI. BACKGROUND: Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT1) and type 2 (AT2) receptors are known to be present in the heart, comparatively little is known about the latter. We therefore examined the role played by AT2 receptors in post-AMI heart failure. METHODS AND RESULTS: In wild-type mice subjected to AMI by coronary artery ligation, AT2 receptor immunoreactivity is upregulated in the infarct and border areas. Among AT2 receptor-null (-/-) mice, the 7-day survival rate after AMI was significantly lower than among wild-type mice (43% versus 67%; P<0.05). All sham-operated animals of both genotypes survived through the study. Ventricular mRNA levels for brain natriuretic peptide were elevated in both genotypes 24 hours after coronary occlusion, with levels in AT2-/- significantly higher than in wild-type mice, as were their lung weights, and histological examination revealed marked pulmonary congestion in the AT2-/- mice. Cardiac function was significantly decreased in AT2-/- mice 2 days after AMI. CONCLUSIONS: AT2 receptor deficiency exacerbates short-term death rates and heart failure after experimental AMI in mice. The AT2 receptor may thus exert a protective effect on the heart after AMI. |
| Author | NAKAO, Kazuwa KAWAKAMI, Rika HORIUCHI, Masatsugu NAKAGAWA, Yasuaki SAITO, Yoshihiko USAMI, Satoru SAITOH, Yoshitomo TANIMOTO, Keiji NAKANISHI, Michio HARADA, Masaki YASUNO, Shinji ADACHI, Yuichiro IWAI, Masaru KISHIMOTO, Ichiro KUWAHARA, Koichiro TAKAHASHI, Nobuki |
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| Snippet | Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1 (AT1) and... Background— Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1... BACKGROUND: Angiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1... BACKGROUNDAngiotensin II plays a prominent role in the progression of heart failure after acute myocardial infarction (AMI). Although both angiotensin type 1... |
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| SubjectTerms | Acute Disease Animals Biological and medical sciences Cardiology. Vascular system Coronary heart disease Disease Models, Animal Disease Progression Echocardiography Electrocardiography Female Heart Heart Failure - diagnosis Heart Failure - etiology Heart Failure - physiopathology Homozygote Ligation Medical sciences Mice Mice, Knockout Myocardial Infarction - complications Myocardial Infarction - diagnosis Myocardial Infarction - physiopathology Natriuretic Peptide, Brain - genetics Natriuretic Peptide, Brain - metabolism Receptor, Angiotensin, Type 1 Receptor, Angiotensin, Type 2 Receptors, Angiotensin - analysis Receptors, Angiotensin - deficiency Receptors, Angiotensin - genetics Receptors, Angiotensin - metabolism RNA, Messenger - metabolism Severity of Illness Index Survival Rate |
| Title | Angiotensin II type 2 receptor deficiency exacerbates heart failure and reduces survival after acute myocardial infarction in mice |
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