In preeclampsia (PE), the action of endothelial nitric oxide (eNO) is reduced by in vitro investigation of characteristic changes using vascular strips of resistance artery. We studied underlying mechanisms in the reduced action of it. The vascular strips of omental resistance arteries were obtained from PE and normotensive pregnant women. Informed consent was obtained from each patient. This study was permitted by ethical board. (1) The various isometric tension by NO were measured by bradykinin (BK), sodium nitroprusside (SNP) and the inhibition of 8-pCPT-cGMPVert@during the STA2 (a stable analogue of thromboxane A2)-induced contraction. (2) The [Ca(2+)]i were measured in the endothelium-intact strip loaded cell-permeable form of Fura 2 (Fura 2-AM). (3) The concentrations of cGMP and eNO synthase (eNOS) were measured in endothelial cell intact strips. (1) In PE, endothelium-dependant (by BK) and -independent (by SNP) relaxation of NO in the STA2-induced contractions were significantly smaller, while the action of c GMP was also reduced. (2) BK increased the concentration of [Ca(2+)]i, although the increase was not reduced in PE. (3) The concentrations of cGMP with BK and without BK and eNOS were not reduced in PE. These results revealed that the action of endothelial NO might be reduced not due to decrease in the production of NO in the endothelium but rather to reduced action of cGMP itself.