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

J Am Soc Nephrol. 2011 Dec;22(12):2187-92. doi: 10.1681/ASN.2010020193. Epub 2011 Oct 21.


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(A) receptor 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Hypertension / etiology
  • Kidney / cytology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Receptor, Endothelin A / physiology*
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / physiology*


  • Receptor, Endothelin A
  • Angiotensin II