The human placenta is vital for the maintenance of normal pregnancy, but mechanisms responsible for the control of vasomotor tone and blood flow within the fetoplacental circulation are poorly characterized. Agonist-induced rhythmical contractions and relaxations (oscillations) in blood vessel tone are a common feature of many vascular beds (1,2), and may allow for an acute regulation of volume flux. Alterations of oscillations may contribute to the pathophysiology of many hypertensive conditions, e.g. pre-eclampsia (PE) (3). Tone oscillations are thought to be influenced by endothelial factors and it is pertinent that PE is associated with endothelial dysfunction (1,3,4). Thus, our aim was to compare the patterns of tone oscillations in placental arteries from women with normal pregnancies and those with PE. Placental biopsies were obtained at term (≥36+6 weeks) from vaginal or Caesarean section (n=4 normal pregnancy) delivery and normalised on a wire myograph at 0.9 of L_5.1kPa and equilibrated in physiological salt solution (37°C; 5%O₂/5%CO₂ ~7%O₂) for 20 min. Following initial exposure to a solution containing 120mM potassium to assess arterial viability, arteries were exposed to the thromboxane-mimetic U46619 (10^-7.5M) for 1 hour. Slow, large amplitude oscillations (>10% of the U46619-induced contraction) were observed in most arteries from women with normal pregnancies (n=15/18) and PE (n=11/15; defined according to international guidelines (4)). All arteries were included in subsequent analysis. Some arteries were exposed to 10^-7.5M U46619 a second time in the presence or absence of the nitric oxide (NO) synthase inhibitor N^G-nitro-L-arginine (L-NNA, 10^-4M). Arteries from women with normal pregnancies developed oscillations with mean±SEM amplitude of 39±7% and frequency of 0.043±0.008 per minute. In the presence of L-NNA (n=6) amplitude was significantly reduced (40±12% to 18±7%, P<0.05, Friedman test), but frequency was unaltered. In arteries from women with PE, the amplitude of oscillations (not frequency) was significantly reduced (17±4%, P<0.01, ANOVA) compared to arteries from women with normal pregnancies. However, in the presence of L-NNA, although the magnitude of the U46619-induced contraction was significantly increased (10.8±1.3kPa to 13.1±1.7kPa, P<0.05, Friedman test, n=8) neither amplitude nor frequency of oscillations were altered. These data indicate that in human placental arteries (i) the patterns of tone oscillations are altered in PE and (ii) NO has a role in mediating tone oscillations in normal pregnancy and the contractile magnitude in PE. These findings may be important when considering regulation of uteroplacental blood flow in normal or pathophysiological pregnancies.