Placental chorionic plate arteries (CPAs) exhibit inconsistent responses to endothelial-dependent dilators [1-3], with minimal relaxation in the short term. Here we tested the hypothesis that long term administration of endothelial-dependent agonists would promote significant relaxation of CPAs. Term placentas (N=11) were obtained post-delivery (vaginal or Caesarean section) from uncomplicated pregnancies. Biopsies were placed into ice-cold HCO₃^–-buffered physiological salt solution (PSS). Arteries were dissected from the chorionic plate, mounted onto a wire myograph, normalised at 0.9 of L_5.1kPa and equilibrated (37°C; 20 min; 5% O₂/5% CO₂ ~7% O₂). Vasoconstriction was assessed with 120mM potassium solution (KPSS). Histamine hydrochloride (HIS), bradykinin (BK) and acetylcholine (ACh; all 10^-6M) were added to pre-contracted vessels (EC₈₀ dose of the thromboxane-mimetic U46619 for 30 min) for 60 min. Experiments with HIS were also performed in the presence of indomethacin (I; 10^-5M), indomethacin plus N^ω-nitro-L-arginine, (IN; both 10^-5M) and indomethacin plus N^ω-nitro-L-arginine in 25mM KCl (INK). Arterial relaxation to donated nitric oxide (NO) was assessed using sodium nitroprusside (SNP; 10^-5M). Normalised luminal internal diameters were 294±18μm (n=44 arteries). Maximal arterial relaxation was 69±3, 86±6 and 95±3% of constriction to U46619 at EC₈₀ concentration with HIS, BK and ACh respectively (Mean +/- SEM; N=5). BK-induced relaxation was transient (100±4% at 60 min) whereas HIS induced a maintained relaxation (74±4% at 60 min; N=5). Maximal arterial relaxation was 68±7%, 76±6%, 79±1%and 86±3% (N=6) of the EC₈₀ U46619-induced contraction respectively (P<0.05; Friedman’s test followed by Dunn’s post hoc test) with HIS alone and in the presence of I, IN and INK, respectively. Arterial relaxation at 60 mins was 71±8%, 84±4%, 89±3% and 92±3% (N=6) of the EC₈₀ U46619-induced contraction, respectively (P<0.05; Friedman’s test followed by Dunn’s post hoc test) with HIS alone and in the presence of I, IN and INK, respectively. 10^-6M HIS but not ACh or BK promotes maintained relaxation of CPAs. This relaxation is partially reduced by blockers of the vascular endothelium. The slower onset of response may relate to ultrastructural features of CPAs, which show well developed endothelial cells, no internal elastic lamina and considerable extracellular matrix separating circularly oriented smooth muscle cells [4].