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Renal denervation prevents renal T cell activation in mice during angiotensin II‐induced hypertension
Author(s) -
Xiao Liang,
Zhang Feng,
Kirabo Annet,
Harrison David G
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb696
Subject(s) - denervation , sympathectomy , medicine , endocrinology , kidney , sympathetic nervous system , renin–angiotensin system , renal artery stenosis , norepinephrine , angiotensin ii , renal artery , renal medulla , blood pressure , dopamine
Increased sympathetic outflow has been implicated in the pathogenesis of hypertension. Recent evidence has also suggested a role of T lymphocytes in hypertension. The link between the central nervous system and immune activation in hypertension is however unclear. We hypothesized that renal sympathetic nerves activate T cells in the kidney in hypertension. We performed unilateral renal denervation in C57BL/6 mice by applying phenol to the left renal artery and cutting large visible nerves. On the same day mice received an osmotic minipump for angiotensin II infusion. Denervation decreased renal norepinephrine content from 162±13 to 42±11 ng/g (p < 0.05) as measured by HPLC. Analysis of T cells was performed using flow cytometry in digested kidneys. T cell (CD3 + ) number was 1.57±0.23×10 5 in the innervated kidney of sham infused mice and this was doubled by Ang II infusion (3.50±0.89×10 5 ). Unilateral renal denervation prevented this increase (1.60±0.31×10 5 vs. intact side, p<0.05) from the same animals. This was accompanied by reduction in the T cell memory marker CD44 and T cell IFN‐γ production. These results suggest a potential role of renal sympathetic nerve traffic linking central command and peripheral inflammation in hypertension. Our data further show that renal sympathectomy might have anti‐inflammatory roles contributing to blood pressure control.