Sex hormone-dependents vascular reactivity is an underlying factor contributing to gender differences in cardiovascular diseases (Sader and Celermajer, 2002). This study evaluated the role of androgens on vascular reactivity in the perfused hind limb preparation in salt – induced hypertension. Thirty six weanling male Sprague – Dawley rats (8 weeks old; weight, 180 – 200)g were either bilaterally orchidectomised (n = 24) or sham-operated (n = 12) (under ketamine and xylazine anaesthesia (90mg and 10mg/kg/body weight i.m) respectively, with or without testosterone replacement (10mg/kg sustanon 250® i.m once in 3 weeks), and were placed on normal (0.3%) or high (4%) NaCl diet for 6 weeks. Arterial blood pressure (BP) was determined via carotid artery cannulation under 25% urethane and 1% α-chloralose anaesthesia (5ml/kg body weight i.p) at the end of the feeding period. Thereafter renal cortical blood flow was measured and renovascular resistance (RVR) was also determined. Vascular responses to PE, ACh and SNP were studied in the perfused hind limb. Fluid balance (FB) and plasma concentration of nitrite (PCN) were also determined. Data were analyzed using one way analysis of variance (ANOVA) and Student-Newman-keuls post Hoc test. Confidence interval was placed at 95%. Rats fed a high salt diet (HSD) showed increases in BP (100±2.0 vs. 124±3.0), RVR (0.29±0.02 vs. 0.34±0.01), FB (5.0±1.34 vs. 9.6±1.83), that was accompanied by decreased plasma nitric oxide (NO) production (0.64±0.09 vs. 0.22±0.05). Orchidectomy reversed but testosterone replacement restored the increased BP (117±2.0 vs. 127±3.0), RVR (0.33±0.01 vs. 0.37±0.01), FB (6.8±1.39 vs. 11.2±1.24) and PCN (0.69±0.15 vs. 0.50±0.04) observed in the rats fed a HSD. High salt diet increased response to PE (60.4±7.61 vs. 84.0±8.63) but this was reversed and restored by orchidectomy and testosterone replacement (70.4±7.13 vs. 79.0±5.34) respectively. HSD also impaired vasorelaxation to ACh (68.8±4.54 vs. 48.4±6.32) and SNP (79.6±5.40 vs. 44.4±8.39). Orchidectomy attenuated the impaired relaxation response to ACh (56.6±4.47 vs. 48.4±3.47) and SNP (64.8±3.60 vs. 58.6±4.14) observed in the HSD fed rats. Testosterone promotes the impairment of vascular function observed in HSD and this may involve the NO pathway.