Cheng J B, Bewtra A J, Townley R G
Arch Int Pharmacodyn Ther. 1985 Jan;273(1):47-61.
Previous studies have shown inconsistent results of the effect of verapamil and nifedipine on airway reactivity. This study was undertaken to determine and compare their effects on the activity of airway muscarinic receptors by contraction experiments and by radioligand receptor binding assays. We found that verapamil (10(-5)-10(-4) M) reduced contraction at rat tracheal muscle to methacholine, a finding consistent with its inhibition on binding of (3H)QNB to bovine tracheal muscle membranes. Unlike verapamil, nifedipine (10(-5)-3 X 10(-5) M) inhibited neither methacholine response nor (3H)QNB binding. Verapamil but not nifedipine decreased the affinity of binding sites. Neither of them affected the concentration of (3H)QNB binding sites. We conclude that the effect of verapamil on airway muscarinic receptor binding sites differs qualitatively from that of nifedipine, and suggests that its effect on the binding sites could account for the inhibitory action of verapamil on airway muscarinic response.
以往的研究表明,维拉帕米和硝苯地平对气道反应性的影响结果不一致。本研究旨在通过收缩实验和放射性配体受体结合试验来确定并比较它们对气道毒蕈碱受体活性的影响。我们发现,维拉帕米(10⁻⁵ - 10⁻⁴ M)可降低大鼠气管肌肉对乙酰甲胆碱的收缩反应,这一发现与其抑制(³H)QNB与牛气管肌肉膜的结合相一致。与维拉帕米不同,硝苯地平(10⁻⁵ - 3×10⁻⁵ M)既不抑制乙酰甲胆碱反应,也不抑制(³H)QNB结合。维拉帕米而非硝苯地平降低了结合位点的亲和力。它们都不影响(³H)QNB结合位点的浓度。我们得出结论,维拉帕米对气道毒蕈碱受体结合位点的影响在性质上与硝苯地平不同,这表明其对结合位点的影响可能是维拉帕米对气道毒蕈碱反应具有抑制作用的原因。