Fetal growth restriction (FGR), a serious pregnancy complication, is associated with raised placental vascular resistance and reduced blood flow which limits nutrient delivery to the fetus. The placenta functions as the fetal lung and, in common with pulmonary vascular disease, FGR is associated with tissue hypoxia. In lung, chronic hypoxia inhibits the expression of Kv1.5, an oxygen-sensitive K channel, which promotes smooth muscle cell (SMC) proliferation and reduces apoptosis, culminating in artery wall remodelling and reduced blood flow1. Placental chorionic plate artery SMCs express Kv1.5 2 but expression in FGR in relation to SMC proliferation and apoptosis remains unexplored. We tested the hypothesis that in FGR chronic hypoxia reduces Kv1.5 expression in SMCs of placental resistance arteries promoting their proliferation and suppressing apoptosis. Placentas were collected at term following normal pregnancy (NP) or FGR (individualised birthweight ratio <5th centile). Serial sections of chorionic plate with underlying villous tissue were examined by immunohistochemistry using antibodies to detect Kv1.5, SMCs (α-actin), endothelial cells (ECs: CD31), proliferation (Ki67) and apoptosis (TUNEL). To examine effects of oxygen on Kv1.5 expression, chorionic plate artery segments (n=83) from normal placentas (N=6) were maintained in culture at 21%, 6% or 1% oxygen (5% CO2, 37°C) for 24, 48 or 72 hr and immunostained for Kv1.5. Kv1.5 staining intensity was scored by 3 persons blinded to sample identity. Proliferation and apoptosis was expressed as the number of positively stained cells as a percent of total cells. Immunostaining of positive control tissue and samples was absent when primary antibody was blocked by antigenic peptide (Kv1.5), replaced with non-immune IgG (α-actin, CD31, Ki67) or in the absence of TdT enzyme (TUNEL). Resistance artery SMCs and ECs showed positive staining for Kv1.5 (co-localised in serial sections). In both NP (N=10 placentas; 162 vessels) and FGR (N=8; 70 vessels), staining intensity was greater in ECs than SMCs (p<0.02; Wilcoxon signed rank) and SMC staining was stronger in large (>300µm) than small (≤100µm) diameter vessels (p<0.01; Kruskal Wallis with Dunns post test). However, there were no differences in EC or SMC Kv1.5 expression, proliferation or apoptosis in FGR compared to NP. Furthermore, Kv1.5 expression in SMC and EC was not altered by exposure of arteries to 21%, 6% or 1% oxygen over 24-72 hr. The similarity in Kv1.5 expression in NP and FGR implies that the channels are not down- regulated by placental hypoxia. This is supported by data showing that SMC Kv1.5 expression in arteries of NP was not suppressed by 72hr exposure to 1% oxygen. The expression of Kv1.5 in SMC and EC implies a functional role for the channel in regulating placental resistance artery tone in both NP and FGR.