Abstract

BackgroundRegulatory T cells (Tregs) have been reported to prevent organ damages in hypertension. This effect might be caused by anti‐inflammatory process. We examined Treg expression and number focusing on spleen where T cells are abundant. The aim of the present study was to determine whether Tregs is altered in the spleen, and blockade of brain Ang II type 1 receptors (AT1R) for central sympathoinhibition affects splenic Tregs in hypertensive rats.Methods and ResultsStroke‐prone spontaneously hypertensive rats (SHRSP) with sympathetic hyperactivity were treated with intracerebroventricular infusion of an AT1R blocker (losartan, 1mg/kg/day for 14 days, ARB) or vehicle (VEH). Wister Kyoto rats (WKY) served as control. Splenic Foxp3 (an essential transcription factor of Tregs) mRNA and CD4+CD25+Foxp3+ cells were lower in SHRSP‐VHE than in WKY (Foxp3 mRNA: 0.47±0.03 vs. 1.02±0.03, P<0.05). Splenic Foxp3 mRNA expression levels were upregulated in ARB‐SHRSP (ARB: 0.44±0.04 vs. VEH: 0.31±0.02, P<0.05), while systolic blood pressure and 24‐hour urinary norepinephrine excretion were decreased. IL‐17 mRNA in the spleen was significantly lower in SHRSP‐ARB than in SHRSP‐VEH (ARB: 0.27±0.04 vs. VEH: 0.47±0.03, P<0.01).ConclusionCentral sympathoinhibition induced by blockade of brain AT1R ameliorates the reduction of splenic Tregs possibly via decreased IL‐17 production in SHRSP.

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