Cardiovascular diseases are among the complications of diabetes mellitus. People with hypertension are encouraged to reduce salt intake. Our working hypothesis is that diabetes will not cause sodium retention in the presence sodium load. This study was carried out to evaluate the role of diabetes in pressure diuresis and natriuresis. Diabetic mice (db/db-/-) 5 week old adult (37-49 g) male and diabetic were purchased from Jackson Laboratory, Bar Harbor, ME, USA. The db/db phenotype spontaneously develops characteristics of type 2 diabetes including obesity, hyperinsulinemia, and insulin resistance. The animals were randomly divided into groups (n=5-6 per group) and assigned to normal rat chow (0.5% NaCl diet) or high salt diet (8% NaCl from Research Diets, Inc. New Brunswick, NJ, USA), for 7 weeks. Renal function was determined by measuring urine volume (Uv), urinary and sodium (UNav). Metabolic cages were used in collecting 24-hr urine samples. Urinary sodium was measured using flame photometer. There were no significant differences in urine volumes collected on Day 1 in high salt and normal salt-fed db/db-/- mice. Urinary volumes (ml) of 26.7±8.1, 18.7±3.9, 28.0±3.5 of high salt-fed mice and 22.5±4.7, 18.2±5.9, 26.0±4.2 of normal salt-fed mice were collected in weeks 1, 3 and 7. The observed weekly increase in urine volume was significant in each group, but not significant between the two groups. Urinary sodium (μmol/ 24 hr) of 16.6±7.1, 22.8±4.1, 66.1±21.3 of high salt-fed mice and 1.0±0.2, 12.5±3.4, 3.5±0.1 of normal salt-fed mice were collected in weeks 1, 3, and 7. There were significant weekly increases in sodium excretion in high salt diet only. From our observation, sodium was excreted significantly. Therefore, sodium retention may not be a contributory factor to the incidence of hypertension in diabetes. There is need for further investigations on the complications of diabetes in relation to cardiovascular events such as hypertension.