Differential Response of Angiotensin II on Interleukin-6 MRNA Expression in Spontaneous Hypertensive and Normotensive Wistar Rats Astrocytes

Atrium

Objective. To determine if Angiotensin (Ang) II differentially affects Interleukin-6 (IL-6) mRNA levels in astrocytes isolated from Spontaneous Hypertensive rats (SHR) as compared to normotensive Wistar rats. Background. Ang II is an effector peptide of the renin angiotensin system that mediates hypertension. It is also a key hormone, growth factor and proinflammatory molecule. IL-6 is a multifunctional cytokine known to mediate inflammatory responses in the body. Ang II has been shown to induce IL-6 secretion from various cell types. In IL-6 knockout mice, Ang II-mediated hypertension is decreased, suggesting a link between Ang II-mediated hypertension and IL-6 expression. Methods. Astrocytes isolated from SHR were used as a genetic hypertension model to examine the effect of Ang II on central IL-6 mRNA expression. These results were compared to astrocytes isolated from normotensive Wistar rats. Astrocytes cultured from cerebellum (CB) and brainstem (BS) regions of the rat brain were treated with 100 nM Ang II time-dependently, and IL-6 mRNA expression measured using quantitative polymerase chain reaction (qPCR). Results. Ang II induced IL-6 mRNA expression in CB and BS astrocytes of both Wistar and SHR rats. However, Ang II's ability to induce IL-6 mRNA expression was greater in Wistar astrocytes as compared to SHR astrocytes at most time points examined. Conclusion. Our findings suggested that in the SHR, the IL-6 pathway may be dysregulated and may represent a nonclassical pathway by which Ang II may contribute to hypertension in this hypertension model Grants. This study was supported by PFRDG grant # 335889