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Decreased T‐regulatory cells are associated with blood pressure elevation and sympathoexcitaton in hypertensive rats (875.10)
Author(s) -
Katsuki Masato,
Hirooka Yoshitaka,
Kishi Takuya,
Sunagawa Kenji
Publication year - 2014
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.28.1_supplement.875.10
Subject(s) - medicine , blood pressure , losartan , angiotensin ii , endocrinology , foxp3 , pathogenesis , blockade , spleen , renin–angiotensin system , angiotensin receptor , receptor , immunology , immune system
Background: Previous reports have suggested that T‐regulatory cells (Tregs) prevent angiotensin II (AngII)‐induced hypertension and organ damage. Abnormal sympathoexcitation is a major factor in the pathogenesis of hypertension. The aim of the present study was to determine whether Tregs are involved in the development of hypertension, and whether blockade of brain AngII type 1 receptors (AT1R)‐induced sympathoinhibition affects Tregs or not. Methods and Results: We examined Tregs in stroke‐prone spontaneously hypertensive rats (SHRSP) at 3 week (early pre‐hypertensive stage), 5 week (late pre‐hypertensive stage), or 15 week (established hypertensive stage) old, and in age‐matched normotensive Wistar‐Kyoto rats (WKY). CD4+CD25+Foxp3+ cells in the spleen and blood did not differ between WKY and early pre‐hypertensive SHRSP, whereas significantly decreased both in late pre‐hypertensive and established hypertensive SHRSP (p<0.05). In established hypertensive SHRSP, intracerebroventricular infusion of losartan (AT1R blocker) for 2 weeks was done to cause depressor response with central sympathoinhibition, and Foxp3 mRNA expression in the spleen was significantly higher than in vehicle‐treated SHRSP. Conclusion: Decreases in T‐Regulatory cells precede blood pressure elevation in SHRSP, thereby Tregs play a key role in the development of hypertension associated with sympathoexcitation.