Fos expression in rat brain during depletion-induced thirst and salt appetite.

Fos expression in rat brain during depletion-induced thirst and salt appetite.
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DOI:
10.1152/ajpregu.1998.274.6.r1807
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发表时间:
1998-06
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
R. Thunhorst;Zhice Xu;M. Cicha;A. Zardetto-Smith;A. K. Johnson
R. Thunhorst;Zhice Xu;M. Cicha;A. Zardetto-Smith;A. K. Johnson
中科院分区:
其他
文献类型:
--
作者:
R. Thunhorst;Zhice Xu;M. Cicha;A. Zardetto-Smith;A. K. Johnson

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Fos 蛋白(Fos 免疫反应性,Fos-ir)的表达在接受血管紧张素依赖性口渴和盐食欲模型的大鼠大脑中进行了绘制。与水和钠摄入相关的生理状态是通过同时皮下注射利尿剂呋塞米(10 mg/kg)和低剂量血管紧张素转换酶(ACE)抑制剂卡托普利(5 mg/kg;Furo/Cap 治疗)产生的。治疗后 2 小时处死动物,并对大脑进行 Fos-ir 处理以评估神经激活。 Furo/Cap 治疗显着增加了已知介导 ANG II 作用的终板和下丘脑结构以及与血容量和压力调节相关的后脑区域的 Fos-ir 密度高于基线水平。 Furo/Cap 治疗通常还使这些结构中的 Fos-ir 密度增加到高于分别施用呋塞米或卡托普利后观察到的水平。已知可阻断大脑中 ACE 作用的卡托普利 (100 mg/kg sc) 剂量在前脑中比后脑区域中 Fos-ir 的减少程度更大。目前的工作提供了进一步的证据,表明终板区域有助于血管紧张素依赖性口渴和盐食欲。
The expression of Fos protein (Fos immunoreactivity, Fos-ir) was mapped in the brain of rats subjected to an angiotensin-dependent model of thirst and salt appetite. The physiological state associated with water and sodium ingestion was produced by the concurrent subcutaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg; Furo/Cap treatment). The animals were killed 2 h posttreatment, and the brains were processed for Fos-ir to assess neural activation. Furo/Cap treatment significantly increased Fos-ir density above baseline levels both in structures of the lamina terminalis and hypothalamus known to mediate the actions of ANG II and in hindbrain regions associated with blood volume and pressure regulation. Furo/Cap treatment also typically increased Fos-ir density in these structures above levels observed after administration of furosemide or captopril separately. Fos-ir was reduced to a greater extent in forebrain than in hindbrain areas by a dose of captopril (100 mg/kg sc) known to block the actions of ACE in the brain. The present work provides further evidence that areas of lamina terminalis subserve angiotensin-dependent thirst and salt appetite.