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Renal tubulointerstitial infiltration of activated T cells and macrophages is invariably present and plays a role in elevation of arterial pressure in nearly all animal models of hypertension (HTN). The role, if any, of elevated renal arterial pressure in the pathogenesis of this inflammatory process is uncertain. Also unclear is whether the cellular infiltration is caused by the local activation of immune cells in the kidney or a consequence of leukocyte activation in the systemic circulation.We studied activation of peripheral blood leukocytes and cellular infiltration in the kidneys of Sprague-Dawley rats with abdominal aorta coarctation (banding) above renal arteries, which causes severe HTN proximal but not distal to coarctation.Compared with the sham operated controls, the aorta-banded group exhibited tubulointerstitial accumulation of activated T cells, macrophages, angiotensin-II positive cells, leukocyte function-associated antigen-1 integrin expressing cells, increased nitrotyrosine abundance (a measure of oxidative stress), and increased macrophage chemoattractant protein-1 in the kidneys which are not exposed to HTN in this model. These findings were associated with the activation of the circulating leukocytes in the aorta-banded animals.Increased baromechanical stress is not a requisite for accumulation of T cells and macrophages in the kidney in the coarctation-induced HTN and possibly in other hypertensive disorders. On the contrary, renal hypoperfusion and the consequent activation of renin-angiotensin system may mediate this process by promoting local induction of chemoattractant and inflammatory cytokines. The observed tubulointerstitial inflammation in this model is associated with leukocyte activation in the systemic circulation. Am J Hypertens 2005;18:1449-1456 © 2005 American Journal of Hypertension, Ltd.