Ontogeny of nitric oxide in the pulmonary vasculature

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

The vasodilator molecule nitric oxide is critically involved in the successful cardiopulmonary transition from fetal to postnatal life. It is produced in the pulmonary endothelium by the endothelial isoform of the enzyme nitric oxide synthase. The expression of endothelial nitric oxide synthase in the lung increases dramatically during late gestation, optimizing the capacity for nitric oxide production at the time of birth. Studies in cultured cell models indicate that the developmental upregulation may be mediated by estrogen, and that the expression of the enzyme is also upregulated by oxygen. Pulmonary endothelial nitric oxide synthase expression is diminished in models of congenital diaphragmatic hernia and neonatal pulmonary hypertension induced by fetal ductal ligation. Thus, there is normally a marked developmental upregulation in endothelial nitric oxide synthase expression in the lung during late fetal life, and attenuated expression of the enzyme may contribute to the pathophysiology of a variety of forms of neonatal pulmonary vascular disease.

Original languageEnglish (US)
Pages (from-to)381-392
Number of pages12
JournalSeminars in Perinatology
Volume21
Issue number5
DOIs
StatePublished - 1997

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Nitric Oxide Synthase Type III
Nitric Oxide
Lung
Up-Regulation
Enzymes
Vasodilator Agents
Vascular Diseases
Pulmonary Hypertension
Nitric Oxide Synthase
Lung Diseases
Endothelium
Ligation
Cultured Cells
Protein Isoforms
Estrogens
Parturition
Oxygen
Pregnancy

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Ontogeny of nitric oxide in the pulmonary vasculature. / Shaul, P. W.

In: Seminars in Perinatology, Vol. 21, No. 5, 1997, p. 381-392.

Research output: Contribution to journalArticle

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