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Angiotensin II‐Induced Neuroinflammation Contributes to Sympathetic Overactivity in Hypertensive Rats.
Author(s) -
Wang Weizhong,
Tan Xing,
Wang Yangkai
Publication year - 2015
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.29.1_supplement.1059.3
Subject(s) - rostral ventrolateral medulla , neuroinflammation , medicine , endocrinology , angiotensin ii , proinflammatory cytokine , blood pressure , angiotensin ii receptor type 1 , sympathetic nervous system , losartan , renin–angiotensin system , heart rate , inflammation
Neuroinflammation has been reported to contribute to cardiovascular dysfunction in hypertension. Increased angiotensin II (Ang II) in the rostral ventrolateral medulla (RVLM) plays an important role in sympathetic overactivity in hypertension. The goal of this present work is to determine the role of Ang II in the RVLM on neuroinflammation in spontaneously hypertensive rats (SHRs). In normotensive WKY rats, intracerebroventricular injection of Ang II (2 weeks) produced a significant increase in blood pressure and renal sympathetic nerve activity, but also increased the content and expression of the proinflammatory sytokine inteleukin‐1 beta, inteleukin‐6, and tumor necrosis factor‐alpha in the RVLM. In SHRs, intracerebroventricular injection of the AT1R antagonist losartan significantly decreased blood pressure and sympathetic outflow, accompanied with reduction in proinflammatory sytokine content and expression. Overexpression of angiotensin‐converting enzyme 2 (ACE2) in the RVLM leads to a significant reduction in blood pressure and sympathetic activity in SHRs. Moreover, mRNA expression of inteleukin‐1 beta, inteleukin‐6, and tumor necrosis factor‐alpha was reduced in SHRs treated with ACE2 overexpression (2 weeks) in the RVLM. Based on the present data, it is suggested that AngII plays an important role in mediating neuroinflammation in the RVLM of hypertensive rats. This work was supported by NSFC (81170240 and 81370363)