Yang R, Jin H, Wyss J M, Chen Y F, Oparil S
Department of Medicine, University of Alabama, Birmingham.
Hypertension. 1992 Aug;20(2):242-6. doi: 10.1161/01.hyp.20.2.242.
We have previously shown that microinjection of monoclonal antibody to atrial natriuretic peptide (ANP) into the caudal nucleus tractus solitarii causes a pressor response in salt-sensitive spontaneously hypertensive rats (SHR) fed a basal (1%) salt diet, suggesting that endogenous ANP in this region may be involved in the centrally mediated regulation of blood pressure in this model. The present study tested the hypothesis that the pressor effect of blocking endogenous ANP in caudal nucleus tractus solitarii is enhanced by dietary salt supplementation in salt-sensitive SHR. Monoclonal antibody to ANP (0.55 micrograms) in 50 nl artificial cerebrospinal fluid or control immunoglobulin G was microinjected into the caudal nucleus tractus solitarii of conscious salt-sensitive SHR, salt-resistant SHR, and Wistar-Kyoto rats fed 1% or 8% salt diets for 3 weeks. Microinjection of the monoclonal antibody into the caudal nucleus tractus solitarii evoked similar increases in mean arterial pressure in salt-sensitive SHR on both 1% and 8% salt diets and in salt-resistant SHR on a 1% salt diet but had no effect in Wistar-Kyoto rats. In contrast, microinjection of control immunoglobulin G into this brain area did not alter mean arterial pressure or heart rate in any experimental group. Thus, endogenous ANP in caudal nucleus tractus solitarii mediates tonic control of blood pressure in both salt-sensitive and salt-resistant SHR but not in Wistar-Kyoto rats, and this effect is independent of the salt sensitivity of hypertension and of dietary salt intake.
我们之前已经表明,将抗心钠素(ANP)单克隆抗体微量注射到孤束核尾侧核,会使喂食基础(1%)盐饮食的盐敏感自发性高血压大鼠(SHR)产生升压反应,这表明该区域的内源性ANP可能参与了此模型中血压的中枢调节。本研究检验了这样一个假设:在盐敏感SHR中,通过补充饮食盐分可增强孤束核尾侧核中阻断内源性ANP的升压作用。将50纳升人工脑脊液中的抗ANP单克隆抗体(0.55微克)或对照免疫球蛋白G微量注射到清醒的盐敏感SHR、盐抵抗SHR以及喂食1%或8%盐饮食3周的Wistar - Kyoto大鼠的孤束核尾侧核中。将单克隆抗体微量注射到孤束核尾侧核后,喂食1%和8%盐饮食的盐敏感SHR以及喂食1%盐饮食的盐抵抗SHR的平均动脉压均有类似升高,但对Wistar - Kyoto大鼠没有影响。相比之下,将对照免疫球蛋白G微量注射到该脑区,在任何实验组中均未改变平均动脉压或心率。因此,孤束核尾侧核中的内源性ANP介导了盐敏感和盐抵抗SHR的血压紧张性控制,但对Wistar - Kyoto大鼠没有作用,并且这种作用与高血压的盐敏感性和饮食盐摄入量无关。