Objective To assess the impact of passive leg movement (PLM) on endothelial function and the underlying molecular mechanisms in Dhal salt-sensitive rat with HFpEF. Methods A total of thirty-two Dahl salt-sensitive male rats, aged seven weeks, were randomly allocated into four groups according to dietary and intervention measures, with eight rats assigned to each group: normal salt, high salt, high salt and passive leg movement group (HS+PLM), high salt and isoflurane group (HS+ISO). HS+PLM and HS+ISO groups rats were fed a high-salt diet for 13 weeks, and randomized to receive PLM or Isoflurane. Diastolic dysfunction was evaluated using invasive hemodynamic measurements and echocardiography. In addition, the in vitro assessment of vascular endothelial function was conducted. Results PLM attenuated deterioration of cardiac diastolic function of rats with HFpEF. Furthermore, PLM resulted in a significant enhancement of vascular endothelium-dependent relaxation to acetylcholine, as well as improvements in aorta remodeling and the dissociation of eNOS dimers in Dahl salt-sensitive rats. PLM also increased expression of p-eNOS. In this model of HFpEF, the endothelial function of the vascular was impaired. However, this was prevented by PLM, which may be associated with alleviating vascular fibrosis and oxidative stress. It also was related to reduced expression of eNOS. Conclusion These results indicate that HFpEF leads to endothelial dysfunction, which can be reversed through PLM