Role of Immune Factors in Angiotensin II-Induced Hypertension and Renal Damage in Dahl Salt-Sensitive Rats

The present study assessed the importance of immunity in AngII (5 ng/kg/min, iv)-mediated hypertension in Dahl Salt Sensitive (SS) rats and SS rats deficient in T- and B-lymphocytes (SS ^Rag1-/-) fed a 0.4% NaCl diet. Baseline mean arterial blood pressure (MAP) was not different between groups. AngII infusion significantly increased MAP in both groups; though MAP increased more rapidly in SS, and the maximal MAP achieved in SS (190±3 mmHg) was significantly greater than that in SS^Rag1-/- (177±3 mmHg) after 12 days. Renal damage, as assessed by albumin excretion rate, was significantly increased after 12 days of AnglI infusion in the SS (from 32±4 to 81±9 mg/day) and in the SS^Rag1-/- (from 12±2 to 51±8 mg/day); albumin excretion rate was significantly different between the SS and SS^Rag1-/- rats at all points measured. Following 9 days of recovery from AngII, MAP was decreased to a greater extent in SS^Rag1-/- (143±5 mmHg) than in SS (157±8 mmHg) when compared to the peak MAP during AngII infusion. At this same time point, the albumin excretion rate of SS^Rag1-/- was significantly lower (42±8 mg/day) than that observed in the SS (66±7 mg/day). Further studies demonstrated that the kidneys of AngII-treated SS had increased CD45+ total leukocytes, CD11b/c+ macrophages/monocytes, and CD3+ T Cells compared to vehicle-treated SS. The present data suggest that infiltrating T cells in the kidney exacerbate renal damage in AngII-induced hypertension in SS rats maintained on a 0.4% NaCl diet, similar to the results observed with a salt stimulus in SS rats.

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