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Vasoprotective Actions of Chronic Vagal Nerve Stimulation in Hypertensive Rats – Role of inflammatory cytokines and vascular migration of inflammatory cells
Author(s) -
Stauss Harald Martin,
Tan Brianna K,
Rotella Diane L,
Ratcliff Jason A,
Harwani Sailesh C,
Chapleau Mark W
Publication year - 2017
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.31.1_supplement.875.8
Subject(s) - endocrinology , medicine , tumor necrosis factor alpha , vasoprotective , inflammation , stimulation , proinflammatory cytokine , ccl2 , chemokine , nitric oxide
In a previous study we demonstrated that four weeks of chronic vagal nerve stimulation (VNS) in stroke‐prone spontaneously hypertensive rats (SHR‐SP) on high‐salt diet prevents progression of endothelial dysfunction and aortic stiffening. This study was designed to test the hypothesis that anti‐inflammatory effects (e.g., reduced activation of inflammatory cells in the spleen, less vascular migration of inflammatory cells) of VNS contribute to these vasoprotective actions of chronic VNS. Aortic collagen I content, determined by immunohistochemistry, was less in SHR‐SP with VNS (n=8) than in sham‐stimulated SHR‐SP (Sham, n=8), confirming the effects of chronic VNS on aortic stiffening. Furthermore, aortic collagen I content correlated with serum levels of the pro‐inflammatory cytokines interleukin‐1 beta (IL‐1β, R=0.77, n=11, P<0.01) and tumor necrosis factor‐alpha (TNF‐α, R‐0.55, n=11, P=0.08). Protein content of the pro‐inflammatory cytokines interleukin‐5 (IL‐5), macrophage inflammatory protein‐1 alpha (MIP‐1α), and TNF‐α was reduced in spleens from SHR‐SP with VNS compared to Sham (IL‐5: 0.35±0.02 vs. 0.69±0.11 pg/mg; MIP‐1α: 0.91±0.04 vs. 1.44±0.13 pg/mg; TNF‐α: 0.18±0.02 vs. 0.28±0.05 pg/mg; n=3 for both groups). Finally, preliminary data based on aortic staining for CD3 (T‐cells), CD45 (leukocytes), and CD68‐positive (macrophages) cells suggest less migration of inflammatory cells into the aorta in VNS compared to Sham (CD3: 25±1% vs. 62±5%; CD45: 28±18% vs. 53±3%; CD68: 23±6% vs. 44±11%; n=2 for both groups; % values are positively stained cells relative to all cells identified by DAPI staining of the cell nuclei). Collectively, these data suggest that reduced splenic activation of inflammatory cells and less vascular migration of inflammatory cells contribute to the vasoprotective actions of chronic VNS in this rat model of severe hypertension. Support or Funding Information Supported by a pilot grant from the University of Iowa Hospitals and Clinics Center for Hypertension Research.