Development of heart failure and congenital septal defects in mice lacking endothelial nitric oxide synthase

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an important role in the regulation of cell growth, apoptosis, and tissue perfusion. Recent studies showed that mice deficient in eNOS developed abnormal aortic bicuspid valves. The aim of the present study was to additionally invest...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2002-08, Vol.106 (7), p.873-879
Main Authors: QINGPING FENG, WEI SONG, XIANGRU LU, HAMILTON, Joel A, MING LEI, TIANQING PENG, YEE, Siu-Pok
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biological and medical sciences
Cardiology. Vascular system
Caspases - metabolism
Congenital heart diseases. Malformations of the aorta, pulmonary vessels and vena cava
Disease Models, Animal
Heart
Heart - embryology
Heart Atria - abnormalities
Heart Atria - enzymology
Heart Atria - pathology
Heart Failure - complications
Heart Failure - enzymology
Heart Failure - genetics
Heart Failure - pathology
Heart Septal Defects - complications
Heart Septal Defects - enzymology
Heart Septal Defects - genetics
Heart Septal Defects - pathology
Heart Ventricles - abnormalities
Heart Ventricles - enzymology
Heart Ventricles - pathology
Heterozygote
Homozygote
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardium - enzymology
Myocardium - pathology
Nitric Oxide Synthase - deficiency
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Survival Rate
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Summary:Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an important role in the regulation of cell growth, apoptosis, and tissue perfusion. Recent studies showed that mice deficient in eNOS developed abnormal aortic bicuspid valves. The aim of the present study was to additionally investigate the role of eNOS in heart development. We examined postnatal mortality, cardiac function, and septum defects in eNOS(-/-), eNOS(+/-), and wild-type mice. Postnatal mortality was significantly increased in eNOS(-/-) (85.1%) and eNOS(+/-) (38.3%) compared with wild-type mice (13.3%, P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.0000024114.82981.EA