Distinct mechanisms underlie the regulation of body fluid balance by neurokinin B and angiotensin II in the rat brain
Distinct mechanisms underlie the regulation of body fluid balance by neurokinin B and angiotensin II in the rat brain
复制标题
神经激肽 B 和血管紧张素 II 在大鼠大脑中调节体液平衡的不同机制
DOI：
10.1016/j.brainres.2011.01.072
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发表时间：
2011
期刊：
影响因子：
2.9
通讯作者：
Inenaga K.
中科院分区：
文献类型：
--
作者：
Asami R;Ono K;Nakanishi O;Inenaga K.
虽然中枢注射神经激动素B(NKB)或血管紧张素II(AngII)引起升压反应，但它们在液体摄入行为中表现出不同的参与。本研究旨在阐明这两种多肽对大鼠体液平衡的调节机制。我们证明脑室注射NKB(1nmo1)和AngII(0.1nmo1)都能引起升压反应。然而，只有血管紧张素转换酶诱导了显著的水摄入量并增加了钠的偏好。联合注射NKB可抑制血管紧张素Ⅱ诱导的钠偏爱，但不影响血管紧张素Ⅱ诱导的水摄入量。神经元活化标志物c-Fos的免疫组织化学结果显示，NKB和AngII均增加了室周器官、下丘脑室旁核和视上核神经元的激活。相反，只有血管紧张素Ⅱ显著增加丘脑室旁核、杏仁中央核(CEA)和终纹腹外侧核(BSTvl)的c-Fos免疫反应。联合注射NKB可抑制血管紧张素Ⅱ诱导的CEA和BSTv1中c-Fos的表达。这些结果表明，中枢注射NKB和AngII通过通过室周器官和下丘脑的神经元通路引起共同的心血管反应，但它们通过不同的途径调节液体摄取行为。这两种多肽对钠偏爱的相反作用可能可以通过它们在CEA和BSTv1中的不同作用来解释，这两种作用都被NKB抑制，并被AngII激活。
Although central injections of either neurokinin B (NKB) or angiotensin II (ANGII) induce a pressor response, they show different involvements in fluid intake behaviors. The aim of the present study was to elucidate the mechanisms by which these two peptides regulate body fluid balance in rats. We demonstrate that intracerebroventricular injections of NKB (1nmol) and ANGII (0.1nmol) both induce pressor responses. However, only ANGII induced significant water intake and increased sodium preference. Co-injection of NKB suppressed the ANGII-induced sodium preference but did not affect the ANGII-induced water intake. Immunohistochemistry for c-Fos, a marker of neuronal activation, revealed that both NKB and ANGII increased neuronal activation in the circumventricular organs and the hypothalamic paraventricular and supraoptic nuclei. In contrast, only ANGII significantly increased c-Fos immunoreactivity in the paraventricular thalamic nucleus, the central amygdala (CeA) and the ventrolateral bed nucleus of the stria terminalis (BSTvl). Co-injection of NKB suppressed the ANGII-induced c-Fos expression in the CeA and BSTvl. These results suggest that centrally injected NKB and ANGII lead to common cardiovascular responses by neuronal pathways through the circumventricular organs and hypothalamus but that they regulate fluid intake behaviors through different pathways. It is likely that the opposing effects of these two peptides on sodium preference can be explained by their differential actions in the CeA and BSTvl, both of which are inhibited by NKB and activated by ANGII.