Activity of the Sympathetic and Renin-Angiotensin-Aldosterone systems play crucial roles in blood pressure response to increased salt intake. This study is on the effect of salt loading in normotensive (NT) and hypertensive (HT) Nigerian subjects and the effects of angiotensin receptor blocker (ARB) and sympathetic excitation on responses of blood pressure and peripheral vascular resistance. Salt was administered orally as 200 mmol of sodium chloride daily for five days (Elias et al , 2014), to 16 NT and 14 HT subjects, that were age matched (39.9±1.3 vs 44.1±2.1yrs). The effect of salt loading on blood pressure and peripheral vascular resistance were then determined, before and after concurrent administration of 50 mg Losartan, an ARB. In addition the responses to 30% Maximum Voluntary Contraction (MVC) by handgrip (HG) for one minute, using a dynamometer were also determined. Blood pressure was measured with a sphygmomanometer and mean arterial blood pressure (MABP, mmHg) was computed. Finger blood flow was determined with a finger plethysmograph (Kura et al, 2008),(AD Instruments) and peripheral vascular resistance (PVR) was calculated from mean arterial blood pressure (MABP) and finger blood flow, in mmHg/mls/s. 24hr urine was also collected. Ethical clearance was obtained from the College’s Ethics Committee. Data are mean+sem, Stats by Students t-test. Urinary Na+ excretion (mmol/24hr) before salt load was 111.4±5.6 in NT and 91.9±14.0 in HT and was increased in both (P<0.05) by salt loading viz, in NT to 176.0±13.8 and in HT to 147.4±19.3. However after salt+Losartan Na+ excretion was virtually the same in NT- 173.2±13.7, but in HT, Na excretion further increased to 182.2±27.0 (P<0.05). For MABP responses to sympathetic excitation by HG: In NT, HG increased MABP by 8.1±1.5% in Controls, by 9.9±1.8% after salt but fell to 7.7±2.1% after salt+losartan. In HT, the corresponding values were 7.9±1.4%, 10.8±1.0% and 8.8±1.1% respectively. HG in NT increased PVR by 25.9±8.1% in control, by 38.0±6.7% after salt and by 22.8±8.8% after salt+losartan and in HT, the corresponding values were 22.9±6.8%, 34.3±10.1% and 32.9±7.5% respectively. The PVR lowering response of Losartan to HG was significantly reduced in NT compared to salt loading (P<0.01) but this was blunted in HT. Thus Losartan ameliorates the MABP response to voluntary hand grip following salt loading in NT and HT comparatively but its effect on PVR response is significantly attenuated in NT but is not reduced in HT. However Losartan increases natriuresis in HT. This may suggest that alteration of PVR by the ARB Losartan, is not majorly responsible for its BP lowering action in salt loaded hypertensive Nigerians.