Abstract 103: Increased Blood Pressure Drives Renal T-cell Infiltration in the Dahl Salt-Sensitive Rat

Abstract

Previous studies have shown that renal T-cell infiltration is a key component of salt-sensitive hypertension in Dahl salt-sensitive (SS) rats. Here we used chronic servo control experiments to determine the contribution of renal perfusion pressure (RPP) to T-cell infiltration in the SS rat kidney. An aortic balloon occluder was placed around the aorta, between the renal arteries, and used to maintain blood pressure to the left kidney at control levels, ~128 mmHg, during 7-days of salt induced hypertension. During the same period, the right kidney was exposed to increased RPP, averaging 158 ± 4 mmHg by high salt (4% NaCl) day-7. The number of infiltrating T-cells was compared between the two kidneys. Renal T-cell infiltration was significantly blunted in the left-servo controlled kidney compared to the right-uncontrolled kidney. The number of mature (CD3+), helper (CD3+CD4+) and cytotoxic T-cells (CD3+CD8+) were all significantly lower in the servo controlled kidney than in the hypertensive kidney (Fig.1). This effect was not specific to T-cells, monocyte, macrophage and B-cell infiltration were all significantly exacerbated in the hypertensive kidney. Increased RPP was also associated with augmented renal injury, with increased protein casts and glomeruli damage in the hypertensive kidney. We conclude that during the development of salt-sensitive hypertension increased RPP contributes to renal T-cell infiltration in SS rats; when blood pressure is maintained at control levels T-cell infiltration is significantly attenuated in the servo-controlled kidney relative to the hypertensive kidney despite exposure to comparable sympathetic drive and circulating factors.