Open AccessVIP/PACAP Signaling as an Alternative Target During Hyperoxic Exposure in Preterm Newborns
Author(s) -
Qëndrim Thaçi,
Shkëlzen Reçica,
Islam Kryeziu,
Vadim Mitrokhin,
Andre Kamkin,
Ramadan B Sopi,
Nikola HadziPetrushev,
Mitko Mladenov
Publication year - 2021
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.934638
Subject(s) - hyperoxia , vasoactive intestinal peptide , bronchopulmonary dysplasia , medicine , nitric oxide , pituitary adenylate cyclase activating peptide , endocrinology , airway , contractility , lung , anesthesia , neuropeptide , biology , receptor , pregnancy , genetics , gestational age
The use of oxygen therapy (high doses of oxygen - hyperoxia) in the treatment of premature infants results in their survival. However, it also results in a high incidence of chronic lung disease known as bronchopulmonary dysplasia, a disease in which airway hyper-responsiveness and pulmonary hypertension are well known as consequences. In our previous studies, we have shown that hyperoxia causes airway hyper-reactivity, characterized by an increased constrictive and impaired airway smooth muscle relaxation due to a reduced release of relaxant molecules such as nitric oxide, measured under in vivo and in vitro conditions (extra- and intrapulmonary) airways. In addition, the relaxation pathway of the vasoactive intestinal peptide (VIP) and/or pituitary adenylate cyclase activating peptide (PACAP) is another part of this system that plays an important role in the airway caliber. Peptide, which activates VIP cyclase and pituitary adenylate cyclase, has prolonged airway smooth muscle activity. It has long been known that VIP inhibits airway smooth muscle cell proliferation in a mouse model of asthma, but there is no data about its role in the regulation of airway and tracheal smooth muscle contractility during hyperoxic exposure of preterm newborns.