Experimental hypertension studies are few in the hooded (Aguti) rat. However, a recent work demonstrated its usefulness for experimental hypertension studies (Mojiminiyi et al. 2005). The present study was designed to investigate some of the mechanisms underlying the development of hypertension in this rat stain during dietary salt and/or L-NAME (N-nitro-L-arginine-methyl-ester) loading. Hypertension was induced in inbred 8 week old hooded rats (n=8 each) by administering 8% salt in the diet for 6 weeks (Sofola et al. 2003) and/or 100 mg/kg/day L-NAME in the drinking water for 4 weeks (Pollock et al. 1993). Urine was collected from the rats weekly, its volume determined and stored. At the end of 6 weeks the blood pressure of the rats was measured invasively following anaesthesia with a 0.25mg/ml urethane and 0.01mg/ml chloralose mixture given intraperitoneally at a dose of 5ml/kg. Blood samples were collected from the rats by cardiac puncture during anaesthesia and serum extracted. The cation concentrations of serum and stored urine samples were measured by flame photometry. Results are presented as mean ± SEM. Statistical analysis was done using one-way ANOVA and a post hoc Student Newman-Keuls test. P< 0.05 was taken as statistically significant. Water consumption, urine volume and Na⁺ excretion increased significantly in salt-loaded and salt+L-NAME groups compared with control (P<0.05) but remained similar in L-NAME rats. These values were however significantly less in salt+L-NAME rats compared with salt loaded rats (P<0.05). Urinary K⁺ excretion and serum Na⁺ and K⁺ concentrations remained similar in the test groups compared to control. The mean arterial pressure (mmHg) increased significantly in the test groups of rats (salt:138.3±4.0; L-NAME: 165.7±6.0; salt+L-NAME: 133.3±5.2) when compared with control (88.4±2.7; P<0.05). These results confirm the earlier finding suggesting the usefulness of the hooded rat for experimental hypertension studies. Attenuation of the diuretic and natriuretic responses to salt loading in the presence of L-NAME suggests that nitric oxide is involved in the mechanisms involved in these responses. It is concluded that nitric oxide deficiency may exacerbate salt and volume retention in salt-loaded hooded rats and possibly play a role in the subtle renal defect underlying salt sensitive hypertension.