Mineralocorticoid Receptors, Neuroinflammation and Hypertensive Encephalopathy

摘要: Worldwide, raised blood pressure is estimated to affect 35-40% of the adult population and a main conditioning factor for cardiovascular diseases stroke. Animal models hypertension have provided great advances concerning pathophysiology human hypertension, as already shown deoxycorticosterone-salt treated rat, Dahl-salt sensitive Zucker obese rat spontaneously hypertensive (SHR). SHR has been widely used study abnormalities brain in chronic hypertension. This review summarises present past evidence that SHR, causes hippocampal tissue damage which triggers pro-inflammatory feedforward cascade affecting this vulnerable region. The driven by mineralocorticoid receptor (MR) activation responding endogenous corticosterone rather than aldosterone. Increased MR expression generalised feature seems support first rise pressure. Then oxidative stress caused vasculopathy hypoxia further increases neurons glia cells, activates microglia mediators, down-regulates anti-inflammatory factors. In contrast MR, involvement glucocorticoid (GR) less certain. GR showed normal levels blockage with an antagonist failed reduce SHR. findings concept MR:GR imbalance switch function towards proverbial "death" receptor.