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首页> 外文期刊>Brain research >Induction of c-fos in forebrain circumventricular organs after renal artery stenosis.
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Induction of c-fos in forebrain circumventricular organs after renal artery stenosis.

机译:肾动脉狭窄后前脑室室器官中c-fos的诱导

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Experiments were done in the anaesthetized rat to determine the effect of activation of renal receptors following renal arterial occlusion (RAO) on the induction of c-fos in neurons of the lamina terminalis in the forebrain. Following RAO, fos labeled neurons were found in both the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Transection of the renal nerves ipsilateral to RAO reduced ( approximately 61%) the number of fos labeled neurons in the SFO and prevented the fos labeling in the OVLT. Similarly, administration of the angiotensin II converting enzyme inhibitor enalapril maleate prior to RAO also reduced ( approximately 27%) the number of fos labeled neurons in the SFO to RAO. However, the number of fos labeled neurons was not altered in the OVLT. The number of fos labeled neurons in the SFO of the intact animals after RAO was found to be greater than the algebraic sum of the number of fos labeled neurons in the renal nerve transected and enalapril treated animals. These results suggest that neurons in the SFO are activated by at least two different mechanisms following renal artery occlusion; those involving the activation of afferent renal nerves and those due to changes in circulating levels of angiotensin II. In addition, afferent renal nerve inputs combined with the effect of increased circulating levels of angiotensin II produce a greater activation of the SFO than either input alone. On the other hand, the OVLT appears to be selectively activated by afferent renal nerve inputs following RAO. Taken together, these data suggest that neural inputs from the kidney may play an important role in controlling body fluid balance and arterial pressure (AP) by influencing the activity of forebrain circumventricular organs neurons that function in the detection of blood borne signals associated with changes in extracellular fluid volume.
机译:在麻醉的大鼠中进行实验,以确定肾动脉闭塞(RAO)后肾受体激活对前脑椎板终末神经元c-fos诱导的影响。在RAO之后,在椎旁器官(SFO)和终板层的器官血管(OVLT)​​中都发现了fos标记的神经元。与RAO同侧的肾神经横切减少了SFO中fos标记的神经元的数量(约61%),并阻止了OVLT中的fos标记。类似地,在RAO之前给予血管紧张素II转化酶抑制剂马来酸依那普利也减少了SFO中RAO的fos标记神经元的数量(约27%)。但是,在OVLT中,fos标记的神经元的数量没有改变。发现RAO后完整动物的SFO中fos标记神经元的数量大于经肾和经依那普利处理的动物中fos标记神经元的数量的代数和。这些结果表明,在肾动脉闭塞后,SFO中的神经元被至少两种不同的机制激活。那些涉及肾传入神经激活的疾病和那些由于血管紧张素II循环水平变化而引起的疾病。此外,肾输入神经输入与血管紧张素II循环水平增加的影响相结合,产生的SFO激活比单独输入任何一种都要强。另一方面,OVLT似乎是由RAO后传入神经神经输入选择性激活的。综上所述,这些数据表明,来自肾脏的神经输入可能通过影响前脑室室器官神经元的活动来控制体液平衡和动脉压(AP),这些活动在检测与血流变化相关的血源性信号中起作用。细胞外液量。

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