Choo L K, Malta E, Mitchelson F
J Pharm Pharmacol. 1986 Dec;38(12):898-901. doi: 10.1111/j.2042-7158.1986.tb03379.x.
The possibility that proadifen (SKF 525A) antagonizes endothelium-dependent relaxations to acetylcholine (ACh) in isolated blood vessel preparations via a muscarinic receptor blocking action has been investigated. In phenylephrine-contracted rat isolated aortic ring preparations (with endothelium), proadifen (10-100 microM) shifts ACh relaxant curves to the right without affecting the maximal response, yet endothelium-dependent relaxations to ATP are unaffected. At lower concentrations, proadifen (1-10 microM) antagonizes negative inotropic responses to ACh and ATP in guinea-pig left atria, antagonizes contractile responses to ACh and elevated [K+] in guinea-pig ileal preparations, displaces (-)-[3H]quinuclidinyl benzilate from muscarinic binding sites in membrane homogenates of guinea-pig ileal longitudinal muscle and reduces contractile responses to elevated [K+] in rat aortic ring preparations. It is concluded that proadifen may possess complex interactions with muscarinic receptors and Ca2+ entry blocking properties in concentrations 10-100 times lower than those reported to inhibit cytochrome P450-catalysed reactions.
已对丙胺太林(SKF 525A)在离体血管制剂中是否通过毒蕈碱受体阻断作用拮抗内皮依赖性乙酰胆碱(ACh)舒张反应进行了研究。在苯肾上腺素收缩的大鼠离体主动脉环制剂(有内皮)中,丙胺太林(10 - 100微摩尔)使ACh舒张曲线右移而不影响最大反应,但对ATP的内皮依赖性舒张反应不受影响。在较低浓度下,丙胺太林(1 - 10微摩尔)拮抗豚鼠左心房对ACh和ATP的负性肌力反应,拮抗豚鼠回肠制剂对ACh和升高的[K⁺]的收缩反应,从豚鼠回肠纵肌膜匀浆中的毒蕈碱结合位点取代(-)-[³H]喹核醇基苯甲酸酯,并降低大鼠主动脉环制剂对升高的[K⁺]的收缩反应。得出的结论是,丙胺太林在浓度比据报道抑制细胞色素P450催化反应的浓度低10 - 100倍时,可能与毒蕈碱受体具有复杂的相互作用以及钙通道阻滞特性。