The presence of myofibroblasts arranged in parallel to the longitudinal axes of anchoring villi of the placenta has previously been described. Furthermore, it has been suggested that intraplacental blood volume, and hence fetal-maternal oxygen-nutrient exchange, may in part be regulated through the longitudinal contraction of anchoring villi. We demonstrate here that anchoring villi have the ability to contract and relax longitudinally. Anchoring villi from normal term human placentae were dissected and suspended from force displacement transducers in order to determine their longitudinal contractility in response to potassium chloride (KCl), N-Nitro -L- arginine methyl ester hydrochloride (L-NAME) and the nitric oxide donors sodium nitroprusside (SNP) and glyceryl trinitrate (GTN). Treatment with both KCl and L-NAME resulted in up to a 62% and 74% increase, respectively, in longitudinal contraction over resting tone. In contrast, both SNP and GTN caused a dose-dependent relaxation of pre-contracted villi. Immunohistochemistry of longitudinal sections of villi confirmed the presence of alpha actin-containing cells in the extravascular space. Histological staining with H & E confirm that the tissues used in these experiments were anchoring villi. These findings suggest that the contraction of anchoring villi may be an important mechanism whereby the placenta may regulate intraplacental volume.