Pirola C J, Balda M S, Alvarez A L, Finkielman S, Nahmod V E
Neuropharmacology. 1986 Dec;25(12):1387-93. doi: 10.1016/0028-3908(86)90113-9.
The lateral septal area was used as a model to study the interaction between acetylcholine (Ach) and bradykinin on arterial blood pressure, since both mediators are present in this region. In the lateral septal area, the administration of the peptide or Ach produced a long-lasting, sympathetic-mediated increase of arterial blood pressure which was blocked by atropine. Pretreatment of the lateral septal area with hemicholinium-3, which depletes stores of acetylcholine, partially blocked the pressor effect of bradykinin but not that of Ach. Captopril--an inhibitor of kininase II--enhanced the pressor effects of bradykinin and Ach. Synaptosomal studies showed that bradykinin increased sodium-dependent, high-affinity uptake of choline and the conversion of [3H]choline to [3H]acetylcholine. Competition experiments using the highly specific muscarinic antagonist [3H]quinuclidinyl benzilate, demonstrated that bradykinin displaced the muscarinic antagonist from its receptor-ligand complexes. These results suggest that in the lateral septal area acetylcholine and bradykinin interact in a positive feed-back which amplifies pressor responses.
由于这两种介质都存在于外侧隔区,因此该区域被用作研究乙酰胆碱(Ach)和缓激肽对动脉血压相互作用的模型。在外侧隔区,注射该肽或Ach会引起由交感神经介导的、持续时间较长的动脉血压升高,而阿托品可阻断这一升高。用半胱氨酸3预处理外侧隔区可耗尽乙酰胆碱储备,该处理可部分阻断缓激肽的升压作用,但不能阻断Ach的升压作用。卡托普利(一种激肽酶II抑制剂)可增强缓激肽和Ach的升压作用。突触体研究表明,缓激肽可增加钠依赖性、高亲和力的胆碱摄取以及[3H]胆碱向[3H]乙酰胆碱的转化。使用高特异性毒蕈碱拮抗剂[3H]喹核醇基苯甲酸酯的竞争实验表明,缓激肽可从其受体-配体复合物中置换出毒蕈碱拮抗剂。这些结果表明,在外侧隔区,乙酰胆碱和缓激肽以正反馈方式相互作用,从而放大升压反应。