Abstract
Elevated blood pressure (BP) and infiltration of the vasculature by monocytes contribute to vascular pathology; but, monocyte migratory characteristics based on differing inflammatory potential under adrenergic activation remains unclear. We compared “non-classical” (CD16++CD14+), “intermediate” (CD16+CD14++), and “classical” (CD16-CD14++) monocyte trafficking and their LPS-stimulated TNF-alpha production in response to a physical stressor (20-min treadmill exercise at 65–70% VO2peak) in participants ( n = 77) with high pre-hypertension (PHT), mild PHT or normal BP (NBP). To determine adrenergic receptor sensitivity, pre-exercise cells were also treated with isoproterenol (Iso) before LPS stimulation. Monocyte subpopulations and intracellular TNF-alpha production were evaluated by flow cytometry. Epinephrine and norepinephrine levels were significantly elevated during exercise. Overall, % non-classical monocytes increased, % intermediate did not change, whereas % classical decreased post-exercise ( p < .001). However, the % increase in non-classical monocytes under adrenergic activation was blunted in PHT individuals ( p < .05). TNF-alpha production in all subsets decreased post-exercise and with in-vitro Iso treatment, irrespective of BP ( p < .001), with nonclassical and intermediate monocytes being a major source of TNF-alpha production. These findings extend our previous reports by showing that the mobilization of “pro-inflammatory” monocytes under sympathoadrenal activation is attenuated with even mild BP elevation. This may be indicative of monocytic adrenergic receptor desensitization and/or greater adhesion of “pro-inflammatory” monocytes to the vascular endothelium in hypertension with clinical implications of vascular pathology.
Published Version
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