Abstract

Perivascular adipose tissue (PVAT) may be a key player in mediating adiposity-associated hypertension because of its proximity to blood vessels. Although increased immune cell occupancy in adipose tissue is proposed to couple adiposity to hypertension, little is known about PVAT’s immune complement. We hypothesized that an immune complement exists in PVAT that would become pro-inflammatory with adiposity-induced hypertension. Male and female Dahl S rats were fed a regular (10% calories from fat) diet (control) or a high fat (60%) diet (HFD) from weaning through 24 weeks of age. HFD rats demonstrated significantly higher systolic blood pressure [mm Hg; control: 127±7 (M), 145±8 (F); HFD: 168±9 (M), 184±11 (F); tail cuff] and visceral adiposity (micro-CT scans). PVATs from the thoracic aorta (APVAT), mesenteric resistance vessels (MRPVAT), non-PVAT retroperitoneal fat (RP fat) and spleen (positive control) were harvested from each animal. T cells (CD4 and CD8), B cells, macrophages, mast cells and neutrophils in the stromal vascular fraction were quantified using 7-color flow cytometry. The type and number of immune cells are presented as a percentage (%) of total live singlet cells. Each immune cell type is reported as % of total immune cells, and CD4, CD8 cells as % of T cells. The table illustrates significant (P<0.05) differences with HFD vs respective controls. HFD-induced hypertension in Dahl S rats leads to greater macrophage infiltration of MRPVAT and RP fat in females vs males. Further studies are needed to gain mechanistic insights into how macrophage subtypes and their associated cytokines in PVAT may alter vascular tone and blood pressure.

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