Vascular Reactivity and Salt Sensitivity in Normotensive and Hypertensive Adults Exaggerated vascular reactivity is a possible mechanism in the development of hypertension and cardiovascular disease (Stewart and France, 2001). Whereas there has been a lot of attention paid to the relationship of dietary salt intake with the development of hypertension there are not many studies designed to study the relationship between vascular reactivity and salt sensitivity in a black population. Fifty-two hypertensive (HT) (age 44.42±1.28y) and forty-seven age-matched normotensive (NT) subjects (age 41.23±1.40y) took part in the study after informed consent was obtained from them. Ethical clearance was obtained from the College of Medicine, University of Lagos. After control parameters were obtained, vascular hyperreactivity was determined as ΔSBP or ΔDBP ≥ +15mmHg in subjects following exposure to the Cold Pressor Test for 1 minute using cold slurry maintained at 4oC (Flaa et al., 2008). Subjects were then salt-loaded with 200mmol Na+/day for 5 days and salt sensitivty determined as earlier (Elias et al., 2011). Test for vascular reactivity was repeated after the salt load. Values are means±SEM, compared with student t test. Salt-loading led to significant increases in systolic blood pressure among the normotensive subjects from 117.5±1.54 mmHg to 121.1±2.1 mmHg (p = 0.03) and among the hypertensive subjects from 144.9±2.6 mmHg to 1519±3.0 mmHg (p = 0.0001); diastolic blood pressure increased significantly only among the hypertensive subjects from 95.73±1.5 mmHg to 100.5± 1.62 mmHg (p = 0.0003). Sytolic and diastolic hyperreactivity were higher among the HT (49% and 39% respectively) compared to NT (44% and 39% respectively) at baseline. However sysstolic hyperreactivity (SHP) increased from 44% to 64% after salt-loading among the NT while diastolic hyperreactivity (DHP) reduced from 39% to 36%. Among the HT, both SHP and DHP reduced from 49% to 33% and from 41% to 31% respectively following salt-loading. Salt sensitivity was higher among HT (56%) compared to NT 34%. Salt sensitivity was positively correlated with systolic reactivity (before salt: r = 0.33; p < 0.05 and after salt: r = 0.25; p > 0.05) but negatively correlated with diastolic reactivity (before salt: r = -0.38; p < 0.05 and after salt: r = -0.40; p < 0.05) among NT. Our results suggest that systolic hyperreactivity may be significant in the development of salt sensitive hypertension among this population.