Satoh T, Karaki H
Department of Veterinary Pharmacology, Faculty of Agriculture, University of Tokyo, Japan.
Jpn J Pharmacol. 1988 Oct;48(2):249-55. doi: 10.1254/jjp.48.249.
Contractile effects of ouabain and K+-free solution on rat aortic strips were investigated. In the aorta without endothelium, application of ouabain or K+-free solution produced, after a latency period, a slow contraction reaching the maximum after 80-100 min. Pretreatment of the muscle with either indomethacin (20 microM) or verapamil (1 microM) decreased the maximum level of these contractions, whereas verapamil, but not indomethacin, prolonged the latency period. Simultaneous application of these inhibitors showed additive inhibitory effects. In the presence of endothelium, the latency period slightly increased without changing the maximum contractile tension. Methylene blue (5 microM) shortened the latency period only in the aorta with endothelium. These results suggest that the contractions of rat aorta induced by ouabain and K+-free solution are due not only to membrane depolarization and Na+-Ca2+ exchange but also to the release of prostaglandins. Endothelium-derived relaxing factor seems to inhibit a part of these contractions.
研究了哇巴因和无钾溶液对大鼠主动脉条的收缩作用。在无内皮的主动脉中，应用哇巴因或无钾溶液，经过一段潜伏期后，会产生缓慢收缩，在80 - 100分钟后达到最大值。用吲哚美辛（20微摩尔）或维拉帕米（1微摩尔）预处理肌肉可降低这些收缩的最大水平，而维拉帕米而非吲哚美辛会延长潜伏期。同时应用这些抑制剂显示出相加的抑制作用。在内皮存在的情况下，潜伏期略有增加，而最大收缩张力不变。亚甲蓝（5微摩尔）仅在有内皮的主动脉中缩短潜伏期。这些结果表明，哇巴因和无钾溶液诱导的大鼠主动脉收缩不仅归因于膜去极化和钠 - 钙交换，还归因于前列腺素的释放。内皮衍生的舒张因子似乎抑制了这些收缩的一部分。
