Lee N H, Forray C, el-Fakahany E E
Department of Pharmacology and Toxicology, University of Maryland School of Pharmacy, Baltimore 21201.
Eur J Pharmacol. 1989 Aug 22;167(2):295-8. doi: 10.1016/0014-2999(89)90591-8.
The cardioselective muscarinic antagonist methoctramine antagonized carbamylcholine-mediated phosphoinositide (PI) hydrolysis in a concentration-dependent fashion in dissociated rat cerebrocortical cells. However, as the concentration of methoctramine was increased above 5 microM, there was a reversal of the antagonism of the PI response. In the absence of carbamylcholine, methoctramine by itself significantly increased PI hydrolysis with a maximal effect at 30 microM. Various classes of receptor antagonists, including atropine, and ion-channel blockers were unable to block methoctramine-stimulated PI hydrolysis.
在离体大鼠大脑皮层细胞中，心脏选择性毒蕈碱拮抗剂甲戊氨酯以浓度依赖方式拮抗氨甲酰胆碱介导的磷酸肌醇（PI）水解。然而，当甲戊氨酯浓度增加至高于5微摩尔时，PI反应的拮抗作用出现逆转。在无氨甲酰胆碱的情况下，甲戊氨酯自身可显著增加PI水解，在30微摩尔时达到最大效应。包括阿托品在内的各类受体拮抗剂以及离子通道阻滞剂均无法阻断甲戊氨酯刺激的PI水解。
