The effects of peptide and nonpeptide antagonists of angiotensin II receptors on the noradrenaline uptake of different brain structures in rats with angiotensin II-induced increase of water intake.

S Stancheva, L Alova, M Velkova, V Georgiev
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Abstract

Angiotensin II (ANG II) significantly increased noradrenaline (NA) uptake by cortical, hypothalamic and hippocampal synaptosomes thus activating noradrenergic neurotransmission. ANG II did not affect NA uptake by striatal synaptosomes. The interaction between AT1 receptors and noradrenergic neurons and the involvement of brain noradrenergic neurotransmitter system in ANG II-induced drinking in rats is suggested by the increase of NA uptake in hypothalamus and frontal cortex which are rich in AT1 receptors and are of importance for drinking behavior. The ANG II-receptor antagonists losartan, EXP 3174, sarmesin and saralasin decreased NA uptake in all brain regions studied as compared to the uptake in the same brain regions of ANG II-injected animals thus antagonising the effect of ANG II. There is no relationship between the inhibition of ANG II-induced water intake and the changes of NA uptake under the effect of the ANG II-receptor antagonists.

血管紧张素II受体多肽和非肽拮抗剂对血管紧张素II诱导的饮水增加大鼠不同脑结构去甲肾上腺素摄取的影响。
血管紧张素II (ANG II)显著增加皮质、下丘脑和海马突触体对去甲肾上腺素(NA)的摄取,从而激活去甲肾上腺素能神经传递。ANGⅱ不影响纹状体突触体对NA的摄取。AT1受体与去甲肾上腺素能神经元的相互作用以及脑去甲肾上腺素能神经递质系统参与了ANG ii诱导的大鼠饮酒,下丘脑和额叶皮层中富含AT1受体,对饮酒行为具有重要意义的NA摄取增加提示了AT1受体与去甲肾上腺素能神经元的相互作用。与注射ANG II的动物相比,ANG II受体拮抗剂氯沙坦、EXP 3174、萨尔米辛和萨拉拉西辛减少了所有脑区NA的摄取,从而拮抗ANG II的作用。在ANG ii受体拮抗剂的作用下,抑制ANG ii诱导的饮水量与NA摄取的变化之间没有关系。
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