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The association between interleukin‑6 (IL‑6) and angiotensin II receptor 1 (AT1‑R) in modulating the progression of heart failure (HF) remains to be fully elucidated. The aim of the present study was to investigate the mechanism of IL‑6 and AT1‑R in a model of HF induced by surgery. Male Sprague‑Dawley rats were randomly divided into five groups, including sham surgery and vehicle groups. The animals were treated for 4 weeks via paraventricular nucleus infusion with either vehicle, losartan (LOS; 200 µg/day), IL‑6 (1 µg/day) or LOS and IL‑6 together (LOS+IL‑6). The rats with HF had higher levels of IL‑6, corticotropin‑releasing hormone (CRH) and norepinephrine (NE), and a lower level of neuronal nitric oxide synthase (nNOS), compared with the rats in the sham surgery group. Treatment with LOS attenuated the decrease in nNOS and the increases in IL‑6, CRH and NE; whereas treatment with IL‑6 facilitated the lower expression of nNOS and higher expression levels of IL‑6, CRH and NE. No differences in the expression levels of nNOS, CRH or NE were found between the LOS group and LOS+IL‑6 group. The results of the study demonstrated that IL‑6 contributed to the progression of HF via the AT1‑R pathway.

molecular medicine reports

Interaction between interleukin-6 and angiotensin II receptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure