Watanabe M
Department of Physiology, Jikei University School of Medicine, Tokyo, Japan.
Pflugers Arch. 1993 Dec;425(5-6):462-8. doi: 10.1007/BF00374873.
Effects of 2,3-butanedione-2-monoxime (BDM) on the contraction of intact and skinned smooth muscles from guinea-pig portal vein were examined. In intact preparations loaded with fura-2, 5-10 mM BDM markedly suppressed Ca2+ transients and force developments induced by 154 mM potassium and by phenylephrine (0.1 mM). On the other hand, in Ca(2+)-free depolarizing solution, BDM did not suppress phenylephrine (0.1 mM)-induced Ca2+ transient and force development. In skinned preparations obtained with Staphylococcus aureus alpha-toxin treatment, BDM did not markedly affect active force development. The above results indicate that BDM suppresses contraction of the portal vein mainly by the inhibition of voltage-dependent cytosolic Ca2+ transients. An additional result suggests that BDM suppresses the force-enhancing effect of alpha 1-adrenergic agents on the contractile elements.
研究了2,3-丁二酮单肟(BDM)对豚鼠门静脉完整平滑肌和去表皮平滑肌收缩的影响。在用fura-2负载的完整标本中,5-10 mM BDM显著抑制由154 mM钾和苯肾上腺素(0.1 mM)诱导的Ca2+瞬变和张力产生。另一方面,在无Ca(2+)的去极化溶液中,BDM不抑制苯肾上腺素(0.1 mM)诱导的Ca2+瞬变和张力产生。在用金黄色葡萄球菌α-毒素处理获得的去表皮标本中,BDM对主动张力产生没有显著影响。上述结果表明,BDM主要通过抑制电压依赖性胞质Ca2+瞬变来抑制门静脉收缩。另一个结果表明,BDM抑制α1-肾上腺素能药物对收缩元件的张力增强作用。