Brain and C-type natriuretic peptide are expressed by the human placenta and are not altered with preeclampsia, fetal growth restriction, or placental hypoxia.

The natriuretic peptide system is a critical regulator of hemodynamic function. Yet its expression in the human placenta has had limited investigation, despite its clear relevance to pregnancy. Preeclampsia and fetal growth restriction are serious conditions of pregnancy, whereby placental dysfunction is central to their pathophysiology. Here, we set out to characterise expression of C-type natriuretic peptide (CNP) and Brain natriuretic peptide (BNP) in human placenta. CNP, BNP, NPR-B and NPR-C expression was assessed in placental tissue from preeclamptic (preterm n = 73; term n = 5), fetal growth restricted (preterm n = 20; term n = 6) and normotensive pregnancies (first trimester n = 11; preterm n = 13; term n = 44). Primary cytotrophoblasts (n = 3) and placental explants (n = 5) were cultured under normoxic (8% O2), or hypoxic (1% O2) conditions and mRNA expression was assessed. In situ hybridisation and immunohistochemistry was performed to localise the expression of NPR-B and NPR-C transcripts, and CNP protein respectively in placenta from first, second and third trimester. CNP, BNP, NPR-B and NPR-C mRNA were expressed in human placenta; their expression was not differentially altered in pathological pregnancies (preeclamptic or fetal growth restricted) or by hypoxia. There was minimal expression of NPR-B and NPR-C, with punctate localisation to the spiral arterioles of first trimester decidua, the cell column, syncytiotrophoblast and cytotrophoblast layer of the placenta. CNP expression was localised to the syncytiotrophoblast. The BNP and CNP system are expressed in human first trimester decidua and placenta throughout gestation; their gene expression was unaltered in pathological placentas and models of placental dysfunction.