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WATER AND ELECTROLYTE HOMEOSTASIS

Renal NF-B activation and TNF- upregulation correlate with salt-sensitive hypertension in Dahl salt-sensitive rats

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi

Submitted 10 March 2006 ; accepted in final form 1 July 2006

Molecular mechanisms of salt-sensitive (SS) hypertension related to renal inflammation have not been defined. We seek to determine whether a high-salt (HS) diet induces renal activation of NF-B and upregulation of TNF- related to the development of hypertension in Dahl SS rats. Six 8-wk-old male Dahl SS rats received a HS diet (4%), and six Dahl SS rats received a low-sodium diet (LS, 0.3%) for 5 wk. In the end, mean arterial pressure was determined in conscious rats by continuous monitoring through a catheter placed in the carotid artery. Mean arterial pressure was significantly higher in the HS than the LS group (177.9 ± 3.7 vs. 109.4 ± 2.9 mmHg, P < 0.001). There was a significant increase in urinary albumin secretion in the HS group compared with the LS group (22.3 ± 2.6 vs. 6.1 ± 0.7 mg/day; P < 0.001). Electrophoretic mobility shift assay demonstrated that the binding activity of NF-B p65 proteins in the kidneys of Dahl SS rats was significantly increased by 53% in the HS group compared with the LS group (P = 0.007). ELISA indicated that renal protein levels of TNF-, but not IL-6, interferon-, and CCL28, were significantly higher in the HS than the LS group (2.3 ± 0.8 vs. 0.7 ± 0.2 pg/mg; P = 0.036). We demonstrated that plasma levels of TNF- were significantly increased by fivefold in Dahl SS rats on a HS diet compared with a LS diet. Also, we found that increased physiologically relevant sodium concentration (10 mmol/l) directly stimulated NF-B activation in cultured human renal proximal tubular epithelial cells. These findings support the hypothesis that activation of NF-B and upregulation of TNF- are the important renal mechanisms linking proinflammatory response to SS hypertension.

nuclear factor-B; tumor necrosis factor-; kidneys; inflammation

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