Ehara T, Hasegawa J, Mitsuiye T
J Mol Cell Cardiol. 1983 Aug;15(8):555-64. doi: 10.1016/0022-2828(83)90331-0.
Catecholamines (isoproterenol, adrenaline, and noradrenaline) elicited a small decrease in the resting potential of guinea-pig ventricular muscle cells depolarized by 27 mM K. This catecholamine-induced depolarization (CAD) was enhanced and often led to an automatic activity, when the membrane shunting conductance was reduced by application of 0.05 to 0.2 mM Ba. CAD was blocked by Mn (1 to 2 mM), verapamil (0.5 to 1 X 10(-5) M), and propranolol (0.1 to 1 X 10(-5) M), but not by phentolamine (10(-5) M). CAD did not develop when both Ca and Ba were absent in the bathing solution, but persisted when Sr was present. These results are consistent with the hypothesis that CAD was due at least partly to an increase in the slow channel conductance that was initiated by catecholamine/beta-receptor interaction. CAD was markedly enhanced at low temperatures (21 to 25 degrees C), and such was characterized by slow repolarization after drug withdrawal. Propranolol, when applied after catecholamine, exerted no appreciable effect on this slow repolarization. This beta-blocker abolished CAD at low temperature, if applied prior to catecholamine. Methylxanthines (2 to 5 mM caffeine or theophylline) produced a depolarization similar to that seen with CAD, and the rate of repolarization after drug withdrawal also slowed at low temperature. The slow repolarization of CAD at low temperature appeared to reflect a slowing in the postreceptor metabolic processes responsible for deactivation of the slow channel that was sensitive to beta-receptor stimulation.
儿茶酚胺（异丙肾上腺素、肾上腺素和去甲肾上腺素）使由27 mM钾引起去极化的豚鼠心室肌细胞的静息电位出现小幅下降。当通过施加0.05至0.2 mM钡使膜分流电导降低时，这种儿茶酚胺诱导的去极化（CAD）增强，且常常导致自动活动。CAD被锰（1至2 mM）、维拉帕米（0.5至1×10⁻⁵ M）和普萘洛尔（0.1至1×10⁻⁵ M）阻断，但不被酚妥拉明（10⁻⁵ M）阻断。当浴液中钙和钡均不存在时，CAD不发生，但当存在锶时则持续存在。这些结果与以下假设一致，即CAD至少部分归因于儿茶酚胺/β受体相互作用引发的慢通道电导增加。CAD在低温（21至25摄氏度）时显著增强，其特征是撤药后复极化缓慢。儿茶酚胺后应用普萘洛尔对这种缓慢复极化无明显影响。如果在儿茶酚胺之前应用，这种β受体阻滞剂在低温下可消除CAD。甲基黄嘌呤（2至5 mM咖啡因或茶碱）产生类似于CAD所见的去极化，且撤药后复极化速率在低温下也减慢。低温下CAD的缓慢复极化似乎反映了负责使对β受体刺激敏感的慢通道失活的受体后代谢过程的减慢。
