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Articles in PresS, published online ahead of print August 22, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00383.2002
Submitted on May 1, 2002
Accepted on August 13, 2002
1 Cardiology Research Laboratory, Lawson Health Research Institute, London Health Sciences Centre, London, Ontario, Canada; Medicine, University of Western Ontario, London, Ontario, Canada
2 Cardiology Research Laboratory, Lawson Health Research Institute, London Health Sciences Centre, London, Ontario, Canada
3 Cardiology Research Laboratory, Lawson Health Research Institute, London Health Sciences Centre, London, Ontario, Canada; Medicine, University of Western Ontario, London, Ontario, Canada; Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada
* To whom correspondence should be addressed. E-mail: qfeng{at}uwo.ca.
We recently demonstrated that mice deficient in endothelial nitric oxide synthase (eNOS) have congenital septal defects and postnatal heart failure. However, mechanisms by which eNOS affects heart development are not clear. We hypothesized that deficiency in eNOS impairs myocardial angiogenesis. Myocardial capillary densities were measured morphometrically in neonatal mouse hearts. In vitro tube formation on Matrigel was investigated in cardiac endothelial cells. In vivo myocardial angiogenesis was performed by implanting Matrigel in the LV myocardium. Myocardial capillary densities and vascular endothelial growth factor (VEGF) mRNA expression were decreased in neonatal eNOS-/- compared with neonatal wild-type mice (P<0.01). Furthermore, in vitro tube formation from cardiac endothelial cells and in vivo myocardial angiogenesis were attenuated in eNOS-/- compared with wild-type mice (P<0.01). In vitro tube formation was inhibited by L-NAME in wild-type mice and restored by NO donor, DETA-NO in eNOS-/- mice (P<0.05). In conclusion, deficiency in eNOS decreases VEGF expression and impairs myocardial angiogenesis and capillary development. Decreased myocardial angiogenesis may contribute to cardiac abnormalities during heart development in eNOS-/- mice.
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