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Pro‐inflammatory action of renin‐angiotensin‐aldosterone system (RAAS) in hypothalamic astrocytes from spontaneously hypertensive rats (SHR)
Author(s) -
Rodriguez Vermali,
Sumners Colin
Publication year - 2012
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.26.1_supplement.891.10
Subject(s) - endocrinology , medicine , renin–angiotensin system , astrocyte , hypothalamus , aldosterone , spontaneously hypertensive rat , microglia , angiotensin ii , chemistry , inflammation , angiotensin ii receptor type 1 , receptor , central nervous system , blood pressure
Over activation of the central RAAS coupled to an enhanced pro‐inflammatory response in the hypothalamic paraventricular nucleus is one of the main contributors to the development and maintenance of neurogenic hypertension. Astrocytes, along with microglia, are key regulators of the central immune response and produce a variety of pro‐inflammatory cytokines including interleukin 6 (IL‐6). Here we demonstrated that incubation of astrocytes purified from the hypothalamus of SHR, a model of neurogenic hypertension, with angiotensin II (Ang II; 100 nM) or aldosterone (ALDO; 100 pM) [both at 3, 6, or 24 h] elicit significantly greater increases in IL‐6 mRNA levels when compared to astrocytes from normotensive rats. Prorenin (PRO; 20 nM) produced similar magnitude increases in IL‐6 mRNA in astrocytes from normotensive rats and SHR, but the effect was more rapid in the latter. Additionally, these RAAS components significantly increased Mas mRNA levels in normotensive rat astrocytes, contrary to their effect in SHR astrocytes, where PRO and ALDO elicited significant decreases in the mRNA for this angiotensin 1–7 (Ang 1–7) receptor. Collectively, these data demonstrate that the pro‐inflammatory actions of RAAS components are enhanced in SHR astrocytes and suggest that there is a reduction in a potential protective mechanism (Ang 1–7/Mas) in these cells in hypertensive rats. Supported by NIH HL‐076803 and HL‐093186.