Baskakov M B, Zheludeva A S, Gusakova S V, Smagliĭ L V, Aleĭnik A N, Ianchuk P I, Medvedev M A, Orlov S N
Fiziol Zh (1994). 2013;59(3):18-24.
Carbon monoxide (CO) is one of a family of gas transmitters. In this article we present the results of mechanographic investigations of the mechanisms of CO action on a rat thoracic aorta segments. We found that relaxing effect of CO donor CORM-2 on vascular smooth muscles is mediated mainly by opening of voltage-dependent potassium channels in smooth muscle cells: 4-aminopyridine, blocking these channels, almost completely eliminated the CO-induced vasorelaxation of the segments precontracted by depolarization of the smooth muscle cells membranes with high potassium (30 mM KCl) solution or by phenylephrine (10 microM). For the first time we documented that CORM-2 reduces the nicardipine-sensitive input of 45Ca2+ in freshly isolated aorta cells. There are reasons to suggest that the L-type voltage-dependent calcium channels of vascular smooth muscle cells are another target for CO, which is implemented in the relaxing effect of this gas transmitter. Additional research is needed to determine the influence of ruthenium complexes (Ru(II)) on phenomenology of carbon monoxide effects.
一氧化碳（CO）是气体递质家族的一员。在本文中，我们展示了对CO作用于大鼠胸主动脉段机制的机械记录研究结果。我们发现，CO供体CORM-2对血管平滑肌的舒张作用主要是通过打开平滑肌细胞中的电压依赖性钾通道介导的：4-氨基吡啶阻断这些通道后，几乎完全消除了CO诱导的、由高钾（30 mM KCl）溶液使平滑肌细胞膜去极化或由去氧肾上腺素（10 microM）预收缩的主动脉段的血管舒张。我们首次记录到CORM-2减少了新鲜分离的主动脉细胞中尼卡地平敏感的45Ca2+内流。有理由认为血管平滑肌细胞的L型电压依赖性钙通道是CO的另一个作用靶点，这在该气体递质的舒张作用中得以体现。需要进一步研究来确定钌配合物（Ru(II)）对一氧化碳效应现象学的影响。
