Fujiwara M, Usui H, Kurahashi K, Jino H, Shirahase H, Mekata F
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Japan.
J Cardiovasc Pharmacol. 1992;20 Suppl 12:S114-6. doi: 10.1097/00005344-199204002-00032.
The present experiments were carried out to investigate the endothelium dependence of the responses to acetylcholine (ACh), arachidonic acid, and histamine in monkey basilar arteries. ACh and arachidonic acid caused endothelium-dependent contraction (EC) in both monkey and canine basilar arteries. The endothelium-derived contracting factor (EDCF) was probably thromboxane A2 (TxA2), as the EDC was attenuated by a cyclooxygenase inhibitor, TxA2 synthetase inhibitors, and TxA2 antagonists. On the other hand, histamine caused endothelium-dependent relaxation (EDR) in monkey and EDC in canine basilar arteries. The EDR in monkey basilar arteries was attenuated by a nitric oxide synthase inhibitor. The EDR and EDC were antagonized by tripelennamine but not by cimetidine, indicating that they are mediated by H1-receptors. From these results, we suggest that in the monkey basilar artery, either there are two types of endothelium (an EDCF type for ACh and arachidonic acid and an EDRF type for histamine) or there is a single type of endothelium with two types of signalling processes (one for EDC and one for EDR).
进行本实验是为了研究猴基底动脉对乙酰胆碱(ACh)、花生四烯酸和组胺反应的内皮依赖性。ACh和花生四烯酸在猴和犬的基底动脉中均引起内皮依赖性收缩(EC)。内皮源性收缩因子(EDCF)可能是血栓素A2(TxA2),因为环氧合酶抑制剂、TxA2合成酶抑制剂和TxA2拮抗剂可减弱EC。另一方面,组胺在猴基底动脉中引起内皮依赖性舒张(EDR),在犬基底动脉中引起EC。猴基底动脉中的EDR可被一氧化氮合酶抑制剂减弱。EDR和EC可被曲吡那敏拮抗,但不能被西咪替丁拮抗,表明它们是由H1受体介导的。根据这些结果,我们认为在猴基底动脉中,要么存在两种类型的内皮(一种是对ACh和花生四烯酸起作用的EDCF型,另一种是对组胺起作用的EDRF型),要么存在一种具有两种信号传导过程的单一类型内皮(一种用于EC,另一种用于EDR)。