Central blockade of salusin β attenuates hypertension and hypothalamic inflammation in spontaneously hypertensive rats

Salusin beta is a multifunctional bioactive peptide and is considered as a promising candidate biomarker for predicting atherosclerotic cardiovascular diseases. The present study was designed to investigate the roles and mechanisms of salusin beta in the paraventricular nucleus (PVN) in attenuating hypertension and hypothalamic inflammation and whether central salusin beta blockade has protective effects in essential hypertension. Normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were used in this study. The rats were chronic PVN infusion either specific salusin beta blocker, antisalusin beta IgG (SIgG), or control IgG (CIgG) for 2 weeks. Hypertensive rats had significantly increased salusin beta expression compared with normotensive rats. Central blockade of salusin beta attenuated hypertension, reduced circulating norepinephrine (NE) levels, and improved cardiac hypertrophy and function in hypertensive rats. Salusin beta blockade significantly reduced proinflammatory cytokines (PICs), nuclear factor-kappa B (NF-kappa B) activity, reactive oxygen species (ROS) levels, and altered renin-angiotensin system (RAS) components in the PVN of hypertensive rats. These findings suggest that the beneficial effects of salusin beta blockade in essential hypertension are possibly due to down-regulate of inflammatory molecules and ROS in the PVN.