Objective: To assess sodium-lithium countertransport (SLC) activity and erythrocyte sodium (ENa) levels in black (Nigerian) hypertensive (HT) patients, normotensive (NT) offspring of hypertensive parents and normotensive offspring of normotensive parents, and to determine if increased SLC activity is related to a familial predisposition to hypertension in black subjects as in Caucasians. Method: The study was done using 60 Nigerian subjects of Edo ethnic origin in three groups of 20 each: (a) untreated new HT patients at the University Teaching Hospital, Benin City; (b) NT children of hypertensive parents (NTHT) traced home and matched for age, sex and body mass index (BMI) with (c) NT children of NT parents (NTNT). SLC activity was measured using a modified method of Canessa et al 1980 and ENa assessed by flame photometry. Results: SLC was markedly higher in both HT patients

Tumor necrosis factor‐alpha (TNFα) is a pro‐inflammatory cytokine that is involved in renal injury associated with salt‐sensitive hypertension (SSH). In the kidney, TNFα receptor type 1 (TNFR1) activation induces natriuresis, suggesting its’ counter‐regulatory role in SSH opposing salt retention. We hypothesize that TNFR1 activity in the kidney is reduced in nitric oxide (NO) deficient condition to facilitate induction of SSH. Experiments were performed in intact (C57BL6 strain) and in 2 models of NO deficient mice: a) chronically treated with NO synthase inhibitor, nitro‐L‐arginine methyl ester (L‐NAME; 0.05 mg/min/g by osmotic mini‐pump), b) eNOS gene knockout (KO) mice, which were fed either normal (NS; 0.4% NaCl) or HS (4% NaCl) containing diet for 4 weeks (n=6‐7 in each group). Systemic blood pressure (SBP) was measured using tail‐cuff plethysmography. The kidneys were isolated and processed for tissue analysis at the end of the experiment. The protein expression of TNFR1 in renal (cortical and medullary) tissues collected from these experimental mice was analyzed using the Western Blot technique. Protein concentration was determined (BCA Assay) using appropriate TNFR1 and GAPDH antibodies. The blot image was quantified with Image J software. HS intake alone did not alter mean SBP in intact mice (NS, 76 ±2.1 vs HS, 78 ±1.4 mmHg) but increased in L‐NAME treated mice (104 ±2.8 mmHg) and in eNOSKO mice (107±3.6 mmHg). The quantitative immunoblot analysis showed that TNFR1 protein level (measured as band intensity density with Image ‐J) was lower in renal cortical (43.9±9.0 vs 110.7±29.8; P<0.05) but not in medullary tissues (114.4±15.5 vs 128.4±97.1; P=n.s.) in L‐NAME treated mice compared to untreated control mice during HS intake condition. The intensity of TNFR1 immunoblot analysis in eNOSKO mice also showed showed the similar results (cortical, 23.7 ± 5.0 vs 110.7±29.8; P<0.001 and medullary, 73.6 ±20.8 vs 128.4±97.1; P=n.s). These data indicate that TNFR1 activity is downregulated in the renal cortical tissues in the condition of NO deficiency. Such downregulation of TNFR1 activity in the renal tubules endowed in cortical tissues (proximal and distal convoluted tubules) would minimize sodium excretion during HS intake leading to the development of SSH in NO deficient conditions.