ET_A activation mediates angiotensin II-induced infiltration of renal cortical T cells

T cells and endothelin (ET-1) both contribute to angiotensin II (AngII)-dependent hypertension. To determine whether ET-1, via the ET _A receptor, facilitates T cell infiltration in the kidney during AngII-dependent hypertension, we measured T cell infiltration in response to four different treatments: saline, AngII infusion, AngII infusion with an ET_A receptor antagonist, or AngII infusion with triple- antihypertensive therapy. After 14 days, AngII increased both BP and the numbers of CD3⁺and proliferating cells in the kidney. Mice treated concomitantly with the ET_Areceptor antagonist had lower BP and fewer CD3⁺ and proliferating cells in the renal cortex. Mice treated with triple therapy had similar reductions in BP but no change in renal cortical CD3⁺ cells compared with kidneys from AngII-infused hypertensive mice. In the outer medulla, both the ET_A receptor antagonist and triple therapy reduced the number of CD3⁺ cells and macrophages. Taken together, these data suggest that ET_A receptor activation in AngII-mediated hypertension increases CD3⁺ cells and proliferation in the renal cortex independent of changes in BP, but changes in the number of inflammatory cells in the renal medulla are BP dependent.