原发性高血压进程中下丘脑内神经元型一氧化氮合酶和血管紧张素Ⅱ1型受体的共表达

Coexpression of neuronal NO synthase and angiotensin Ⅱ type 1 receptor in the hypothalamus in hypertensive condition

目的：观察Wistar-Kyoto（WKY）大鼠和自发性高血压大鼠（SHR）下丘脑室旁核（PVN）和视上核（SON）内神经元型一氧化氮合酶（nNOS）和血管紧张素Ⅱ1型受体（AT-1R）的共表达,以及加压素（AVP）和nNOS基因水平的表达差异.方法：应用免疫荧光双标染色结合RT-PCR技术.结果：SHR和WKY大鼠PVN和SON内都有大量的nNOS和AT-1R免疫阳性神经元分布并部分共存,但SHR组nNOS和AT-1R共存率明显高于对照组.与之一致,SHR组PVN和SON内nNOS和AVP mRNA含量都高于对照组.结论：在高血压发病进程中,NO发生代偿性增加,可部分负反馈抑制中枢肾素-血管紧张素系统,但这种抑制不能完全逆转过度激活的血管紧张素Ⅱ和AVP.

Objective： To investigate the colocalization and expression of neuronal NO synthase （nNOS） with Angiotensin ]] 1 type receptor （AT-1R） as well as arginine vasopressin （AVP） and nNOS mRNA in the hypothalamic nuclei of Wistar-Kyoto （WKY） and spontaneously hypertensive rats （SHR）. Methods： The dual immunofluorescence staining combined with RT- PCR technology were used. Results： We found there were a quantity of nNOS and AT-1R immunoreactive neurons in the paraventricular nucleus （PVN） and supraopticnucleus （SON）. The ratios of coexistence varied in the hypothalamus of SHR and WKY rats, and that of SHR was higher than WKY rats. We found that the nNOS mRNA and AVP mRNA levels were up-regulated in the SHR group. Conclusion~ Nitric oxide （NO） might act as an inhibitory regulator of the activity of RAS in response to hypertension, but the repression cannot reverse the over-activity of Angiotensin ]I and AVP.