钙通道参与神经降压素而非乙酰胆碱的收缩活性：用钙通道阻滞剂和Bay K 8644对大鼠胃底进行的研究。
Involvement of calcium channels in the contractile activity of neurotensin but not acetylcholine: studies with calcium channel blockers and Bay K 8644 on the rat fundus.
作者信息
Donoso M V, Huidobro-Toro J P, Kullak A
出版信息
Br J Pharmacol. 1986 Aug;88(4):837-46. doi: 10.1111/j.1476-5381.1986.tb16257.x.
The contractile activity of neurotensin and acetylcholine on rat isolated fundus strips was examined in preparations maintained in Tyrode buffer containing 2.5, 1.0 or 0 mM Ca2+. While the neurotensin contractions depended markedly on the external Ca2+ concentration, the acetylcholine-induced muscular responses were not significantly affected by omission of calcium in the superfusion media. Pre-incubation of rat fundus strips with nifedipine (0.03-3.8 microM), diltiazem (0.5-3.5 microM) or methoxyverapamil (0.3-1.3 microM) antagonized in a non-surmountable fashion the contractile activity of neurotensin but not of acetylcholine. Pretreatment with Bay K 8644 potentiated in a concentration-dependent fashion the contractile activity of rat fundus strips to neurotensin without modifying to any significant degree the acetylcholine-induced contractions. Nifedipine blocked in a concentration-dependent manner the Bay K 8644-induced potentiation of the neurotensin contractile responses in the fundus. Results demonstrate the dependence on external calcium of the contractile activity of neurotensin and the resistance of the muscarinic response to external calcium manipulations. The coupling of the neurotensin receptor to calcium channels is discussed.
在含有2.5、1.0或0 mM钙离子的台氏缓冲液中维持的大鼠离体胃底条上，检测了神经降压素和乙酰胆碱的收缩活性。虽然神经降压素引起的收缩明显依赖于细胞外钙离子浓度，但超灌流液中钙离子缺失对乙酰胆碱诱导的肌肉反应没有显著影响。用硝苯地平（0.03 - 3.8 microM）、地尔硫卓（0.5 - 3.5 microM）或甲氧基维拉帕米（0.3 - 1.3 microM）预孵育大鼠胃底条，可不可逾越地拮抗神经降压素的收缩活性，但对乙酰胆碱的收缩活性无影响。用Bay K 8644预处理以浓度依赖方式增强大鼠胃底条对神经降压素的收缩活性，而对乙酰胆碱诱导的收缩没有显著改变。硝苯地平以浓度依赖方式阻断Bay K 8644诱导的胃底条中神经降压素收缩反应的增强。结果表明神经降压素收缩活性对细胞外钙离子的依赖性以及毒蕈碱反应对细胞外钙离子操作的抗性。讨论了神经降压素受体与钙通道的偶联。
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