Role of angiotensin‐converting enzyme gene polymorphism in persistent pulmonary hypertension of the newborn

Abstract

Angiotensin-converting enzyme gene polymorphism did not impact the risk or severity of PPHN among infants ≥ 34 weeks GA.

Analysis of nitric oxide synthase gene polymorphisms in neonatal respiratory distress syndrome among the Chinese Han population

“…Moreover, the 6A3 allele of surfactant protein A1(SP-A1) was less common among preterm infants with RDS and was absent among those with severe RDS, which suggests a possible protective role for this allele or other genes with which it is in linkage disequilibrium in RDS [11]. Glutathione-S-transferase-P1 (GSTP1) I105V polymorphism and Angiotensin converting enzyme (ACE) gene deletion/deletion polymorphism have also been reported to be protective factors for respiratory distress in preterm infants, and another study showed that angiotensin-converting enzyme gene polymorphism did not impact the risk or severity of persistent pulmonary hypertension of the newborn among infants >34 weeks GA [16-18]. Many of these associations with RDS have not been tested in multiple independent populations or have not been consistently replicated across studies.…”

The ontogeny of human pulmonary angiotensin‐converting enzyme and its aberrant expression may contribute to the pathobiology of bronchopulmonary dysplasia (BPD)

“…ACE is predominantly expressed in the pulmonary microvascular endothelial cells, which is in contrast to that of other organs where ACE is expressed in the arteries . The most AT‐II conversion via ACE within the body occurs during pulmonary blood perfusion . Because of the angiogenic function of AT‐II, ACE has been suggested to play a role in vascular remodeling, pulmonary hypertension and in the pathomechanism of neonatal lung diseases .…”

“…7,8 The most AT-II conversion via ACE within the body occurs during pulmonary blood perfusion. 9 Because of the angiogenic function of AT-II, ACE has been suggested to play a role in vascular remodeling, pulmonary hypertension 10 and in the pathomechanism of neonatal lung diseases. [11][12][13][14] ACE inhibitor ingestion during pregnancy has been linked to human pulmonary hypoplasia as part of a general ACE-induced fetopathy.…”