Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis.

@article{Zhao2002DeficiencyIE,
  title={Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis.},
  author={Xue Zhao and Xiangru Lu and Qingping Feng},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2002},
  volume={283 6},
  pages={
          H2371-8
        }
}
  • Xue Zhao, Xiangru Lu, Q. Feng
  • Published 1 December 2002
  • Biology, Medicine
  • American journal of physiology. Heart and circulatory physiology
We recently demonstrated that mice deficient in endothelial nitric oxide (NO) synthase (eNOS) have congenital septal defects and postnatal heart failure. However, the 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… 
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References

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TLDR
The data demonstrate that eNOS plays an important role in normal heart development and results in heart failure and congenital septal defects during cardiac development, which is associated with increases in cardiomyocyte apoptosis.
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TLDR
These results show a strong association between eNOS deficiency and the presence of a bicuspid aortic valve, providing the first molecular insight into one of the most common types of congenital cardiac abnormality.
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TLDR
It is demonstrated that acute inhibition of eNOS reveals a role for NO in setting the basal coronary vascular tone as well as participation in reactive hyperemia and the response to ACh, and chronic inhibition of NO formation in eNos-/- mutant mice induces no changes in basal coronary flow and reactiveyperemia, suggesting the activation of important compensatory mechanisms.
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TLDR
It is suggested that defective endothelial NO synthesis may limit angiogenesis in patients with endothelial dysfunction related to atherosclerosis, and that oral L-arginine supplementation constitutes a potential therapeutic strategy for accelerating angiogenic in Patients with advanced vascular obstruction.
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TLDR
Hydralazine prevented hypertension and arteriolar rarefaction in adult mice, suggesting a non-NO-dependent pathway and the lack of eNOS did not affect microvascular densities in either of the muscles studied.
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TLDR
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TLDR
Increased NO production from iNOS expression contributes to myocardial dysfunction and mortality after MI in mice.
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TLDR
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TLDR
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TLDR
It is concluded mice deficient for eNOS show characteristically abnormal prenatal and postnatal development including fetal growth restriction, reduced survival, and an increased rate of limb abnormalities.
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