肾缺血引起大鼠儿茶酚胺神经元Fos表达

实验应用Fos蛋白和酪氨酸羟化酶（tyrosine hydroxylase,TH）的双重免疫组化方法,观察肾脏动脉阻断（renal artery occlusion,RAO）是否激活脑干中核团的儿荷酚胺能神经元。所得结果如下：（1）脑干中Fos样蛋白的基础性表达低;RAO可诱发孤束核（nucleus tractus solitarius,NTS）、最后区（area postrema,AP）、巨细胞旁外侧核（paragi-gantocellularis lateralis,PGL）和蓝斑（locus coeruleus,LC）核团中许多神经元显示Fos样免疫反应（Fos-like immunoreactivi-ty,FLI）。（2）NTS、AP、PGL和LC核团中含有较多的儿茶酚胺能神经元;RAO能激活其中的部分儿荷酚胺能神经元。（3）腺苷受体阻断剂8－苯茶碱可明显减弱RAO所致的上述效应。以上结果表明,肾脏短暂缺血能激活脑干内的一些神经核团以及其中的部分儿荷酚胺能神经元。此效应可能是肾缺血时腺苷释放作用于肾内腺苷受体后引起肾传入神经活动增加的结果。

Renal ischemia-induced Fos expression in catecholaminergic neurons of rats

The present study was undertaken to define whether the renal artery occlusion (RAO) would activate the catecholaminergic neurons in the brainstem nuclei by double immunohistochemical method for detecting Fos and tyrosine hydroxylase. The results are as follows: (1) while the basal expression of Fos was relatively low in the brainstem, RAO was capable of inducing a robust Fos-like immunoreactive neurons in the nucleus tractus solitarius (NTS), area postrema (AP), nucleus paragigantocellularis lateralis (PGL) and locus coeruleus (LC); (2) numerous catecholaminergic neurons in NTS, AP, PGL and LC could be activated by RAO as shown by Fos expression; and (3) these responses to RAO were significantly attenuated by pretreatment with an adenosine receptor antagonist 8-phenyltheophylline. The results suggest that RAO can activate a large number of neurons including some catecholaminergic neurons in the brainstem nuclei. Such effects of renal ischemia may be attributed to RAO-induced adenosine release from the kidney which subsequently activates renal afferents.