哌唑嗪对自发性高血压大鼠下丘脑nNOS表达的影响  

Effects of prasozin on the expression of nNOS in the hypothalamus of spontaneous hypertensive rats

作　　者：朱永红[1] 童明[1] 张露青[1] 肖明[1] 丁炯[1] 

机构地区：[1]南京医科大学人体解剖学系,江苏南京210029

出　　处：《解剖学研究》2010年第2期96-99,109,共5页Anatomy Research

基　　金：江苏省自然科学基金(BK2006232)

摘　　要：目的研究哌唑嗪延缓自发性高血压大鼠(SHR)病理生理进程是否与调控下丘脑内神经元型一氧化氮合酶(nNOS)的表达有关。方法 8周龄雄性SHR,持续给予哌唑嗪1个月后,检测平均动脉压(MAP)和心率(HR)以及进行肾脏组织化学染色,并应用免疫荧光染色结合显微图像分析及Western blot测定下丘脑nNOS的表达水平。结果与未给药同龄SHR相比,给药SHR组MAP和HR明显降低,肾脏纤维化损害程度减轻,下丘脑nNOS蛋白水平升高,室旁核和视上核内nNOS阳性神经元含量增加,但均未达到正常同龄Wistar大鼠水平。结论哌唑嗪可能通过调节下丘脑nNOS发挥中枢降压作用,进而部分逆转自发性高血压发病进程。Objective To explore whether prasozin attenuates the pathophysiological progress of spontaneous hypertensive rats （SHR） via regulating expression of neruonal nitric oxide synthase （nNOS） in the hypothalamus. Methods Eight-week SHR were treated with prazosin for 1 month. Then, the mean arterial pressure （MAP） and heart rate （HR） were measured and histoehemistry of the kidney was analyzed. Immunofluorescence staining combined with micrograph analysis and western-blotting detection were performed to evaluate expression levels of nNOS in the hypothalamus. Results Compared with untreated SHR, SHR received prazosin had low levels of MAP and HR, and attenuated renal fibrosis. Furthermore, SHR exhibited increases in number of nNOS positive neurons in the PVN, SON and nNOS protein levels in the hypothalamus. However, all of the above parameters did not reach normal levels in Wistar rats. Conclusion Prasozin may play central depressive role by regulating nNOS in the hypothalamus, which subsequently partially reverse the spontaneous hypertensive progress.

关 键 词：自发性高血压大鼠 室旁核 视上核 神经元型一氧化氮合酶 原发性高血压 哌唑嗪 

分 类 号：R544.1[医药卫生—心血管疾病]