Abstract
BackgroundAt birth, the release of surfactant from alveolar type II cells (ATIIs) is stimulated by increased activity of the beta-adrenergic/adenylyl cyclase/cyclic 3′-5′ adenosine monophosphate-signaling cascade. Atrial natriuretic peptide (ANP) stimulates surfactant secretion through natriuretic peptide receptor A (NPR-A). ANP inhibits adenylyl cyclase activity through its binding to NPR-C. We wished to further understand the role of the NPR-C in perinatal transition.MethodsWe studied ATII expression of NPR-C in fetal and newborn sheep using immunohistochemistry, and surfactant secretion in isolated ATIIs by measuring 3 [H] choline release into the media.ResultsANP induced surfactant secretion, and, at higher doses, it inhibits the stimulatory effect of the secretagogue terbutaline. ATII NPR-C expression decreased significantly after birth. Premature delivery also markedly decreased ANP and NPR-C in ATIIs. Co-incubation of terbutaline (10 -4 M) with ANP (10 -6 M) significantly decreased 3 [H] choline release from isolated newborn ATII cells when compared with terbutaline alone; this inhibitory effect was mimicked by the specific NPR-C agonist, C-ANP (10 -10 M).ConclusionANP may act as an important epithelial-derived inhibitor of surfactant release in the fetal lung, and downregulation of ANP and NPR-C following birth may sensitize ATII cells to the effects of circulating catecholamines, thus facilitating surfactant secretion.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 349-355 |
| Number of pages | 7 |
| Journal | Pediatric Research |
| Volume | 82 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 1 2017 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health
Cite this
Natriuretic peptide C receptor in the developing sheep lung : Role in perinatal transition. / Mathew, Bobby; D'angelis, Christopher A.; Lakshminrusimha, Satyanarayana; Nickerson, Peter A.; Sokolowski, June J.; Kumar, Vasantha H.S.; Wang, Huamei; Wynn, Karen A.; Holm, Bruce A.; Ryan, Rita M.
In: Pediatric Research, Vol. 82, No. 2, 01.08.2017, p. 349-355.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Natriuretic peptide C receptor in the developing sheep lung
T2 - Role in perinatal transition
AU - Mathew, Bobby
AU - D'angelis, Christopher A.
AU - Lakshminrusimha, Satyanarayana
AU - Nickerson, Peter A.
AU - Sokolowski, June J.
AU - Kumar, Vasantha H.S.
AU - Wang, Huamei
AU - Wynn, Karen A.
AU - Holm, Bruce A.
AU - Ryan, Rita M.
PY - 2017/8/1
Y1 - 2017/8/1
N2 - BackgroundAt birth, the release of surfactant from alveolar type II cells (ATIIs) is stimulated by increased activity of the beta-adrenergic/adenylyl cyclase/cyclic 3′-5′ adenosine monophosphate-signaling cascade. Atrial natriuretic peptide (ANP) stimulates surfactant secretion through natriuretic peptide receptor A (NPR-A). ANP inhibits adenylyl cyclase activity through its binding to NPR-C. We wished to further understand the role of the NPR-C in perinatal transition.MethodsWe studied ATII expression of NPR-C in fetal and newborn sheep using immunohistochemistry, and surfactant secretion in isolated ATIIs by measuring 3 [H] choline release into the media.ResultsANP induced surfactant secretion, and, at higher doses, it inhibits the stimulatory effect of the secretagogue terbutaline. ATII NPR-C expression decreased significantly after birth. Premature delivery also markedly decreased ANP and NPR-C in ATIIs. Co-incubation of terbutaline (10 -4 M) with ANP (10 -6 M) significantly decreased 3 [H] choline release from isolated newborn ATII cells when compared with terbutaline alone; this inhibitory effect was mimicked by the specific NPR-C agonist, C-ANP (10 -10 M).ConclusionANP may act as an important epithelial-derived inhibitor of surfactant release in the fetal lung, and downregulation of ANP and NPR-C following birth may sensitize ATII cells to the effects of circulating catecholamines, thus facilitating surfactant secretion.
AB - BackgroundAt birth, the release of surfactant from alveolar type II cells (ATIIs) is stimulated by increased activity of the beta-adrenergic/adenylyl cyclase/cyclic 3′-5′ adenosine monophosphate-signaling cascade. Atrial natriuretic peptide (ANP) stimulates surfactant secretion through natriuretic peptide receptor A (NPR-A). ANP inhibits adenylyl cyclase activity through its binding to NPR-C. We wished to further understand the role of the NPR-C in perinatal transition.MethodsWe studied ATII expression of NPR-C in fetal and newborn sheep using immunohistochemistry, and surfactant secretion in isolated ATIIs by measuring 3 [H] choline release into the media.ResultsANP induced surfactant secretion, and, at higher doses, it inhibits the stimulatory effect of the secretagogue terbutaline. ATII NPR-C expression decreased significantly after birth. Premature delivery also markedly decreased ANP and NPR-C in ATIIs. Co-incubation of terbutaline (10 -4 M) with ANP (10 -6 M) significantly decreased 3 [H] choline release from isolated newborn ATII cells when compared with terbutaline alone; this inhibitory effect was mimicked by the specific NPR-C agonist, C-ANP (10 -10 M).ConclusionANP may act as an important epithelial-derived inhibitor of surfactant release in the fetal lung, and downregulation of ANP and NPR-C following birth may sensitize ATII cells to the effects of circulating catecholamines, thus facilitating surfactant secretion.
UR - http://www.scopus.com/inward/record.url?scp=85027341789&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85027341789&partnerID=8YFLogxK
U2 - 10.1038/pr.2017.40
DO - 10.1038/pr.2017.40
M3 - Article
C2 - 28288148
AN - SCOPUS:85027341789
VL - 82
SP - 349
EP - 355
JO - Pediatric Research
JF - Pediatric Research
SN - 0031-3998
IS - 2
ER -