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饮食性钠缺乏期间大鼠下丘脑和室周器官中的血管紧张素II受体结合

Angiotensin II receptor binding in the rat hypothalamus and circumventricular organs during dietary sodium deprivation.

作者信息

Yamada H, Mendelsohn F A

机构信息

Department of Medicine, Austin Hospital, University of Melbourne, Heidelberg, Australia.

出版信息

Neuroendocrinology. 1989 Oct;50(4):469-75. doi: 10.1159/000125265.

Abstract

The effect of dietary sodium intake on angiotensin II (Ang II) receptor binding in the rat brain was studied using quantitative in vitro autoradiography. After 2 weeks of sodium deprivation, the peripheral angiotensin system was activated as shown by increased plasma renin activity (4-fold) and plasma aldosterone concentration (approximately 40-fold). At the same time, Ang II receptor binding in the adrenal glomerulosa zone increased by 40%. Frozen brain sections prepared from 12 male Sprague-Dawley rats (6 control, 6 sodium-deprived) were incubated with 125I[Sar1, Ile8] Ang II, exposed to X-ray film, and Ang II receptor binding in individual brain nuclei was quantitated by computerized densitometry. Ang II binding in the area postrema was significantly suppressed in the sodium-deprived rats (60% of control; p less than 0.05). No change was observed in the other circumventricular organs studied, the subfornical organ or organum vasculosum of the lamina terminalis. Ang II binding in the solitary tract nucleus was not affected by the dietary salt treatment. In the hypothalamic paraventricular nucleus, there was a small (9%) but significant (p less than 0.001) increase in Ang II receptor binding in the sodium-deprived group. However, no change was observed in the hypothalamic median preoptic or suprachiasmatic nuclei, areas with similarly high Ang II receptor binding. These results suggest that only a limited subset of brain Ang II receptors respond to sodium deprivation and do so in a region-specific manner. These results support evidence that the central angiotensin system may contribute to the regulation of fluid and electrolyte homeostasis.

摘要

采用定量体外放射自显影术研究了膳食钠摄入量对大鼠脑内血管紧张素II(Ang II)受体结合的影响。钠缺乏2周后,外周血管紧张素系统被激活,表现为血浆肾素活性增加4倍,血浆醛固酮浓度增加约40倍。同时,肾上腺球状带的Ang II受体结合增加了40%。从12只雄性Sprague-Dawley大鼠(6只对照,6只钠缺乏)制备的冰冻脑切片与125I[Sar1,Ile8]Ang II孵育,曝光于X射线胶片,通过计算机密度测定法定量单个脑核中的Ang II受体结合。钠缺乏大鼠的最后区Ang II结合显著受抑(为对照的60%;p<0.05)。在所研究的其他室周器官,即穹窿下器官或终板血管器中未观察到变化。孤束核中的Ang II结合不受膳食盐处理的影响。在钠缺乏组,下丘脑室旁核的Ang II受体结合有小幅度(9%)但显著(p<0.001)的增加。然而,在下丘脑视前正中核或视交叉上核中未观察到变化,这些区域的Ang II受体结合同样很高。这些结果表明,只有有限的一部分脑Ang II受体对钠缺乏有反应,且以区域特异性方式作出反应。这些结果支持了中枢血管紧张素系统可能参与体液和电解质稳态调节的证据。

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