室旁核中的Salusin-β可通过血管加压素升高高血压大鼠的血压和促进交感神经活性外流

Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing 210029, China

AimsSalusin-β is a bioactive peptide with peripheral hypotensive, mitogenic and pro-atherosclerotic effects. The present study was designed to determine the roles of salusin-β in the paraventricular nucleus (PVN) and its relationship with arginine vasopressin (AVP) in hypertension and sympathetic activation.Methods and resultsRenovascular hypertension was induced by two-kidney, one-clip (2K1C) in male Sprague-Dawley rats. Acute experiments were carried out 4 weeks after 2K1C or sham-operation under urethane and alpha-chloralose anaesthesia. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) were recorded. Microinjection of salusin-β into the PVN increased the RSNA, MAP, and HR in a dose-related manner, whereas anti-salusin-β IgG in the PVN decreased the RSNA and MAP, and abolished the effects of salusin-β in 2K1C rats. However, either salusin-β or anti-salusin-β IgG in the PVN failed to cause any significant effects in sham-operated rats. The number of salusin-β-like immunopositive neurons in the PVN was significantly increased in 2K1C rats. Salusin-β in the PVN increased the plasma AVP and norepinephrine levels in 2K1C rats, but not in sham-operated rats. Iv injection of dTyr(CH 2)5(Me)AVP (an AVP V1-receptor antagonist, AAVP) decreased RSNA and MAP, and abolished the effects of salusin-β in the PVN in 2K1C rats. Microinjection of AAVP into the rostral ventrolateral medulla (RVLM), but not into the PVN, abolished the effects of salusin-β on RSNA and HR.ConclusionSalusin-β in the PVN increases blood pressure, heart rate, and sympathetic outflow via both circulating AVP and AVP in the RVLM in hypertensive rats. © 2013 Published on behalf of the European Society of Cardiology. All rights reserved.

Zhu, G.-Q.; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing 210029, China; email:gqzhucn@njmu.edu.cn