AT1受体在脑内胆碱能刺激引起的钠水排泄反应中的作用

目的和方法 :本工作通过整体实验和免疫组化的方法 ,观察脑血管紧张素能AT1受体在侧脑室注射氨甲酰胆碱引起的促钠排泄反应中的作用和下丘脑室旁核TH IR的变化。结果 :用脑血管紧张素能AT1受体阻断剂Losar tan( 2 0 μg)预处理 ,可部分阻断侧脑室注射氨甲酰胆碱引起的促钠排泄反应和利尿作用 (P <0 .0 5)。免疫组化实验显示侧脑室给予氨甲酰胆碱后 40min ,下丘脑室旁核 (PVH)、室周核 (Pe)、弓状核 (Arc)和下丘脑前区后部 (AHP)的酪氨酸羟化酶 (TH )免疫反应活性明显增强。Losartan预处理后侧脑室再注射氨甲酰胆碱 ,除PaPo的免疫反应活性未发生明显变化外 ,上述其余神经核团的TH免疫反应活性明显下降。结论 :在脑胆碱能刺激引起的钠水排泄反应中有AT1受体的参与 ;阻断脑血管紧张素能AT1受体对胆碱能刺激引起Arc、Pe和AHP的儿茶酚胺能神经元兴奋性有下调作用。提示脑血管紧张素能和儿茶酚胺能神经通路在下丘脑室旁核等脑区共同参与介导了脑内胆碱能刺激引起的促钠排泄反应 ,同时血管紧张素能神经元还影响儿茶酚胺能神经元的功能活动

The role of brain AT1 receptor in renal sodium and water excretion and the change of TH-IR in hypothalamus

Aim and Methods:To investigate the role of modulation by angiotensin A T 1 receptor in sodium and water excretion induced by cholinergic agonist carba chol. Thyrosine hydroxylase immunoreactivity (TH-IR) in hypothalamus were also observed. Results: The natriuretic and diuretic effect induced b y carbachol (CBC) were partially inhibited by pretreatment of losartan, a specif ic blocker of angiotensin AT 1 receptor (P<0.05). Immunohistochemistry show ed that both TH-IR density and number of TH-IR positive neurons were markedly increased in PaPo, Arc, Pe and AHP of hypothalamus at 40 min after carbachol adm inistration, as compared with NS group (P<0.05). However, in losartan pretre ated group, the number and the density of TH-IR were significantly decreased in such nuclei mentioned above except PaPo. Conclusion: The result s above suggest that brain AT 1 receptor appears to be involved in mediating na triuresis induced by cholinergic stimulus. The blockade of AT 1 receptor may down regulate the excitability of adrenergic neurons in Arc, Pe and AHP induced by CBC. We postulate that brain adrenergic and angiotensinergic pathway get invo lved in natriuresis induced by brain cholinergic stimulus together. Moreover, an giotensinergic neurons may influence the activity of adrenergic neurons in hypot halamus.