Abstract: Objective To explore the mechanism of vascular function by maternal exposure to lipopolysaccharide（LPS）in adult offspring rats. Methods Nulliparous pregnant and time-matched SD rats were randomly divided into two groups:control group and LPS group（n=6for each group）. Saline or LPS（0.79mg/kg）were administered intraperitoneally on the pregnant day 8,10and 12. All offspring rats were weaned at 4weeks of age. Blood pressure was measured noninvasively by the tail-cuff method at 9,11,13and 15weeks of age. Mesenteric vascular reactivity in response to angiotensinⅡ（AngⅡ,10-10-10-5 mol/L）and protein level of angiotensinⅡtype 1receptor（AT1R）were determined by Westen blot,respectively. Results The systolic blood pressure in the postnatal offsprings treated with LPS rats was higher than that of control group at 9,11,13and 15weeks of age（109.6±2.6）vs（102.9±2.5）,（117.7±1.5）vs（108.1±3.3）,（128.1±3.6）vs（117.2±2.1）,（135.1±3.2）vs（123.0±2.3）mm Hg,respectily,all P＜0.01),the maximum constriction response to AngⅡin the third-grade branches of mesenteric arteries（8.5±0.4）vs（3.5±0.3）mNand the AT1R protein expression of mesenteric arteries（1.21±0.08vs 0.75±0.08,all P＜0.05）were increased at the age of 15weeks in rat offsprings after maternal exposure to LPS.Conclusion The increased AT1R protein expression and augmented response to AngⅡin mesenteric arteries maybe involve in the pathogenesis of hypertension in the adult rat offsprings following maternal exposure to LPS.