Den Hertog A, Pielkenrood J, Ras R, van den Akker J
Eur J Pharmacol. 1984 Feb 17;98(2):223-34. doi: 10.1016/0014-2999(84)90593-4.
The role of calcium and potassium in the alpha-action of adrenaline in pulmonary artery and portal vein was compared with that in taenia caeci by measuring changes in membrane potential, muscle contraction and ion fluxes in quiescent preparations from guinea-pigs (23 degrees C). The depolarization evoked by adrenaline (5 x 10(-8)-3 x 10(-5) M) was sustained in portal vein; in pulmonary artery it declined to a constant level after reaching an initial maximum. In calcium-free medium (20 min) containing EGTA (0.4 mM) and high magnesium (6.2 mM) adrenaline did not affect the membrane potential or the contractile state of the portal vein. Under these conditions the sustained phase of the response was abolished in the pulmonary artery; the remaining transient depolarization and contraction could be evoked only once. Adrenaline (3 x 10(-5) M) caused an increased 45Ca loss and 86Rb loss from the pulmonary artery and taenia caeci in calcium-free solution; a second addition of adrenaline to the calcium-free solution did not enhance the 45Ca loss from these tissues. The portal vein responded with an enhanced 86Rb loss on addition of the alpha-agonist. The bee toxin apamin (3 x 10(7) M) did not modify the depolarization, the contraction or the 45Ca and 86Rb fluxes evoked by adrenaline in the blood vessels. Enhancement of the 86Rb loss from taenia in the presence of adrenaline was prevented by apamin, but the excess loss of 45Ca was not abolished. It is concluded that adrenaline enhances cytoplasmic calcium by promoting calcium entry from the extracellular space in portal vein. In pulmonary artery and taenia caeci this is accompanied by mobilization of calcium from a cellular structure. Calcium entry facilitates triggering of the contractile proteins in vascular smooth muscle and is associated with membrane depolarization; in taenia caeci the mobilization of calcium caused by alpha-receptor activation is associated with the opening of potassium channels producing hyperpolarization and accordingly relaxation of the smooth muscle cells.
通过测量豚鼠（23摄氏度）静态标本中的膜电位、肌肉收缩和离子通量，比较了钙和钾在肾上腺素对肺动脉和门静脉的α作用中的作用，以及它们在盲肠带中的作用。肾上腺素（5×10⁻⁸ - 3×10⁻⁵ M）引起的门静脉去极化持续存在；在肺动脉中，它在达到初始最大值后下降到一个恒定水平。在含有EGTA（0.4 mM）和高镁（6.2 mM）的无钙培养基（20分钟）中，肾上腺素不影响门静脉的膜电位或收缩状态。在这些条件下，肺动脉反应的持续阶段被消除；剩余的短暂去极化和收缩只能被诱发一次。肾上腺素（3×10⁻⁵ M）在无钙溶液中导致肺动脉和盲肠带的⁴⁵Ca损失和⁸⁶Rb损失增加；向无钙溶液中再次添加肾上腺素并没有增强这些组织的⁴⁵Ca损失。添加α激动剂时，门静脉的反应是⁸⁶Rb损失增加。蜜蜂毒素蜂毒明肽（3×10⁻⁷ M）不改变肾上腺素在血管中引起的去极化、收缩或⁴⁵Ca和⁸⁶Rb通量。蜂毒明肽可防止肾上腺素存在时盲肠带中⁸⁶Rb损失的增加，但不能消除⁴⁵Ca的过量损失。结论是，肾上腺素通过促进门静脉中细胞外空间的钙内流来增加细胞质钙。在肺动脉和盲肠带中，这伴随着钙从细胞结构中的动员。钙内流有助于触发血管平滑肌中的收缩蛋白，并与膜去极化相关；在盲肠带中，α受体激活引起的钙动员与钾通道的开放有关，导致超极化，从而使平滑肌细胞松弛。
