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

Abstract

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.

• Authors: Erika I Boesen, Karthik R Krishnan, Jennifer S Pollock, David M Pollock
• Journal: Journal of the American Society of Nephrology : JASN (J Am Soc Nephrol) Vol. 22 Issue 12 Pg. 2187-92 (Dec 2011) ISSN: 1533-3450 [Electronic] United States
• PMID: 22021713 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Receptor, Endothelin A
• Angiotensin II

Topics

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