Lipsius S L, Vassalle M
Eur J Pharmacol. 1977 Sep 1;45(1):35-44. doi: 10.1016/0014-2999(77)90055-3.
Possible adrenergic mechanisms involved in acetylcholine (ACh) induced potassium movements in the sinus node have been investigated using a tracer potassium (42K) and a microelectrode technique. The ACh-induced increase in 42K uptake was enhanced by propranolol and was unaffected by phentolamine. Reserpinization neither prevented the ACh-induced increase in 42K uptake nor the enhanced effect in the presence of propranolol. In reserpinized preparations, ACh-induced 42K uptake was the same before and after norepinephrine (NE) administration, but was greater after acute reserpinization. NE alone induced an increase in 42K uptake but the simultaneous administration of ACh and NE provoked an increase in 42K uptake similar to that obtained with ACh alone. When both neuromediators and atropine were given simultaneously, an increase in 42K uptake did not occur. Thus, the ACh induces an increase in 42K uptake independently of NE. ACh antagonizes the NE effect on 42K uptake independently of a muscarinic interaction.
利用示踪钾(42K)和微电极技术,研究了窦房结中可能参与乙酰胆碱(ACh)诱导钾离子移动的肾上腺素能机制。普萘洛尔增强了ACh诱导的42K摄取增加,而酚妥拉明对此无影响。利血平化既未阻止ACh诱导的42K摄取增加,也未阻止普萘洛尔存在时的增强作用。在利血平化的制剂中,去甲肾上腺素(NE)给药前后ACh诱导的42K摄取相同,但急性利血平化后更高。单独使用NE可诱导42K摄取增加,但同时给予ACh和NE会引起与单独使用ACh时相似的42K摄取增加。当同时给予神经介质和阿托品时,未出现42K摄取增加。因此,ACh可独立于NE诱导42K摄取增加。ACh可独立于毒蕈碱相互作用拮抗NE对42K摄取的影响。