Abstract
Microglia are activated in the paraventricular nucleus (PVN) of the hypothalamus, where they may contribute to the release of proinflammatory cytokines (PIC) that stimulate sympathoexcitatory systems. In this study we determined whether blockade of AT1‐R (valsartan), or inhibition of microglial activation (minocycline) or angiotensin‐converting enzyme (captopril) attenuates PIC in heart failure (HF) rats. Adult male Sprague‐Dawley rats were subjected to coronary artery ligation to induce HF or sham surgery (SHAM). Subsequently, animals were orally treated with valsartan (VAL, 30mg/kg/day), minocycline (MIN, 10mg/kg/day) or captopril (50mg/kg/day) for 4 weeks. Immunohistochemistry revealed activation PIC in the microglial cells and PVN neurons of HF rats compared with SHAM. Oral treatment with VAL, MIN or captopril inhibited microglial activation and attenuates PIC in the PVN of HF rats. Treatment with VAL, MIN or captopril also reduced plasma levels of NE and PIC. These findings suggest that activated microglia in the paraventricular nucleus of hypothalamus contribute to the pathogenesis of heart failure.
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