ETA 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(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.
Experimental Medicine, Georgia Health Sciences University, Augusta, GA 30912, USA. dpollock@georgiahealth.edu
Erika I
EI
Boesen
Karthik R
KR
Krishnan
Jennifer S
JS
Pollock
David M
DM
Pollock
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D006973:Hypertension / Q000209:etiology; D007668:Kidney / Q000166:cytology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D044022:Receptor, Endothelin A / Q000502:physiology*; D013601:T-Lymphocytes / Q000187:drug effects* / Q000502:physiology*
D044022:Receptor, Endothelin A; D000804:Angiotensin II