Den Hertog A, Van den Akker J
Eur J Pharmacol. 1987 Jun 4;137(2-3):233-9. doi: 10.1016/0014-2999(87)90227-5.
The effect of procainamide (2.0-5.0 mM) and quinidine (0.2-1.0 mM) on the alpha 1 response evoked by adrenaline (3 X 10(-6) M) in smooth muscle cells of guinea-pig taenia caeci (22 degrees C) was studied in the presence of yohimbine (3 X 10(-6) M), propranolol (3 X 10(-6) M) or atropine (10(-6) M). The electrotonic potential elicited by the application of a constant current to the preparation was slightly increased (about 10%) by procainamide (5.0 mM) but not by quinidine (1.0 mM). The double-sucrose gap method was used for measurements. The alpha 1 response evoked by adrenaline in the absence of extracellular calcium (15 min) was represented by a transient hyperpolarization of the muscle cells, while the hyperpolarization elicited in the presence of calcium was sustained. The hyperpolarization is caused by enhancement of the potassium efflux assumed to be linked with mobilization of calcium form a cellular structure. Superfusion of the preparation with calcium-containing solution to replenish the calcium store in the presence of procainamide (10 min) before the alpha 1 response evoked in the absence of calcium and procainamide did not affect the transient hyperpolarization. Quinidine, however, suppressed the alpha 1 response when the same procedure was followed. Both the transient and the sustained hyperpolarization evoked in smooth muscle cells in the presence of procainamide (15 min) or quinidine in calcium-containing or in calcium-free solution, respectively, were inhibited. The alpha 1 response was reflected by a depolarization of the muscle cells after the potassium channels had been blocked with apamin (3 X 10(-7) M, 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)
在育亨宾（3×10⁻⁶ M）、普萘洛尔（3×10⁻⁶ M）或阿托品（10⁻⁶ M）存在的情况下，研究了普鲁卡因胺（2.0 - 5.0 mM）和奎尼丁（0.2 - 1.0 mM）对豚鼠盲肠带平滑肌细胞中肾上腺素（3×10⁻⁶ M）诱发的α₁反应的影响（22℃）。向标本施加恒定电流所引发的电紧张电位，在加入5.0 mM普鲁卡因胺时略有增加（约10%），但加入1.0 mM奎尼丁时则无变化。采用双蔗糖间隙法进行测量。在无细胞外钙（15分钟）时，肾上腺素诱发的α₁反应表现为肌肉细胞的短暂超极化，而在有钙存在时诱发的超极化则持续存在。这种超极化是由假定与从细胞结构中动员钙相关的钾外流增强所引起的。在无钙且无普鲁卡因胺诱发α₁反应之前，用含钙溶液对标本进行灌流以补充钙储备（10分钟），同时加入普鲁卡因胺（10分钟），这并不影响短暂超极化。然而，按照相同步骤操作时，奎尼丁会抑制α₁反应。在含或不含钙的溶液中，分别加入普鲁卡因胺（15分钟）或奎尼丁后，平滑肌细胞中诱发的短暂和持续超极化均受到抑制。在用蜂毒明肽（3×10⁻⁷ M，20分钟）阻断钾通道后，α₁反应表现为肌肉细胞的去极化。（摘要截选至250字）
