ROLE OF ANGIOTENSIN-II IN BROWN ADIPOSE THERMOGENESIS DURING COLD-ACCLIMATION
ROLE OF ANGIOTENSIN-II IN BROWN ADIPOSE THERMOGENESIS DURING COLD-ACCLIMATION
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DOI：
10.1152/ajpendo.1993.265.6.e860
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发表时间：
1993-12-01
影响因子：
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通讯作者：
CASSIS, LA
中科院分区：
文献类型：
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作者：
CASSIS, LA
研究了血管紧张素 II (ANG II) 在寒冷诱导的棕色脂肪组织 (BAT) 产热过程中观察到的交感神经效应机制增强的作用。冷暴露（4 摄氏度）7 天会导致每克湿重或每个 ISF 叶的肩胛间脂肪 (ISF) ANG II 含量增加，但肾素-血管紧张素系统的血浆成分没有随之变化。此外，在预载[H-3]去甲肾上腺素 (NE) 的 ISF 切片中，与环境温度对照相比，ANG II (10 nM) 导致冷暴露大鼠 ISF 切片诱发的 H-3 溢出增加（3 倍）。然而，尽管来自冷暴露大鼠的 ISF 切片中的基础 H-3 流出量增加（2 倍），但来自冷暴露大鼠和对照大鼠的 ISF 切片中诱发的 H-3 溢出没有差异。冷暴露大鼠 ISF 切片中 [H-3]NE 的特异性神经元摄取减少了 64%。对冷暴露的大鼠施用非肽 AT1 受体拮抗剂氯沙坦可完全抑制 ANG II 介导的突触前促进 ISF 切片诱发的 H-3 溢出。然而，氯沙坦给药对寒冷诱导的 ISF 中 ANG II 含量、蛋白质含量的增加和神经元 [H-3]NE 摄取的减少没有影响。这些研究的结果表明，寒冷诱导的 BAT 生热作用会导致突触前 ANG II 促进 NE 释放的改变以及从突触间隙去除 NE 的缺陷（神经元摄取），这两者都会增强交感神经系统介导的生热作用。此外，这些结果表明 ANG II 在 BAT 中冷诱导产热的交感神经活动增强中发挥作用。
The role of angiotensin II (ANG II) in increased sympathetic neuroeffector mechanisms observed in cold-induced thermogenesis of brown adipose tissue (BAT) was examined. Cold exposure (4-degrees-C) for 7 days resulted in an increase in interscapular fat (ISF) ANG II content expressed per gram wet weight or per lobe of ISF, without concomitant changes in plasma components of the renin-angiotensin system. Additionally, in ISF slices preloaded with [H-3]norepinephrine (NE), ANG II (10 nM) resulted in an increase (3-fold) in evoked H-3 overflow from ISF slices from cold-exposed rats compared with ambient temperature controls. However, although basal H-3 outflow was increased (2-fold) in ISF slices from cold-exposed rats, evoked H-3 overflow was not different between ISF slices from cold-exposed and control rats. Specific neuronal uptake of [H-3]NE in ISF slices from cold-exposed rats was decreased by 64%. Administration of the nonpeptide AT1-receptor antagonist losartan to cold-exposed rats resulted in complete inhibition of ANG II-mediated presynaptic facilitation of evoked H-3 overflow from ISF slices. However, losartan administration had no effect on cold-induced increases in ANG II content, protein content, and decreases in neuronal [H-3]NE uptake in ISF. Results from these studies suggest that cold-induced thermogenesis of BAT results in alterations in presynaptic ANG II facilitation of NE release and defects in removal of NE from the synaptic cleft (neuronal uptake), both of which would enhance sympathetic nervous system-mediated thermogenesis. Furthermore, these results demonstrate a role for ANG II in enhanced sympathetic activity of cold-induced thermogenesis in BAT.