Heritability of salt-sensitive hypertension and high susceptibility of offspring’s blood pressure (BP) to maternal perinatal high salt diet (HSD) [Gray et al., 2015; Maruyama et al., 2015] suggests that hypertension has its origin early in life. However, the initiating factor for early origin of salt-sensitive hypertension and the mechanism(s) that underlie it is not clear. To investigate the mechanism(s) underlying the foetal programming of salt-sensitive hypertension, pregnant Sprague-Dawley rats were exposed to perinatal normal (0.3%) or high (8%) salt diet from day 1 of pregnancy till term. The following experiments were conducted in the offspring at 12 weeks of age: Blood pressure (BP) was measured via arterial cannulation under urethane and α-chloralose anesthesia (5ml/kg body weight i.p) using ADinstrument powerlab. Isolated abdominal aorta reactivity to noradrenaline (NA) and acetylcholine (ACh) in the presence or absence of endothelial nitric oxide synthase (eNOS) inhibition by L- nitro arginine (L-NA) was determined and serum concentrations of C-reactive proteins (CRP), TNF-α and IL-6 was measured using commercially available kits. Mean arterial BP was elevated (p< 0.05) in the offspring of dams exposed to perinatal HSD (116±3 vs. 103±2 mmHg). Maximum contractile response to noradrenaline was similar (72.22±5.57% vs. 79.45±5.76%) in both groups of offspring of dams fed a normal and high salt diet respectively. However, maximum relaxation response to acetylcholine with (54.23±3.92 vs. 39.45±3.98%) or without L-NA (84.23±4.92 vs. 61.32±4.76%) was significantly reduced in the offspring of dams that were exposed to HSD. Perinatal HSD elevated CRP (511.7±13.52 vs. 771.7±25.74ng/ml), IL-6 (112.5±2.7 vs. 120.8±2.43pg/ml) and TNF-α (2200±123.8 vs. 3900±198.3pg/ml) in the offspring. Findings from this study suggest that perinatal feeding of HSD to the dams elevated BP in the offspring by increasing vascular tone as well as systemic and vascular inflammation.