2,3-丁二酮单肟（BDM）可诱导犬心肌肌浆网释放钙。

2,3-Butanedione 2-monoxime (BDM) induces calcium release from canine cardiac sarcoplasmic reticulum.

作者信息

Phillips R M, Altschuld R A

机构信息

Department of Medical Biochemistry, Ohio State University, Columbus 43210, USA.

出版信息

Biochem Biophys Res Commun. 1996 Dec 4;229(1):154-7. doi: 10.1006/bbrc.1996.1772.

DOI:10.1006/bbrc.1996.1772

PMID:8954098

Abstract

2,3-Butanedione 2-monoxime (BDM) is a well known inhibitor of skeletal and cardiac muscle contraction. Recently, it has been discovered that BDM has an influence on the sarcoplasmic reticulum (SR). We investigated the effects of BDM on the SR in our digitonin lysed myocyte system, which measures accumulated SR Ca2+. While BDM (30 mM) had no effect on SR Ca2+ uptake (under conditions that included Ca2+ release channel efflux inhibitors), it induced SR Ca2+ release (no efflux inhibitors) with a maximal reduction of 72% of SR Ca2+ at pCa 6.0. A titration showed that even 5 mM BDM resulted in a 45% reduction at that same pCa. Also, a positive correlation was found between the degree of BDM induced Ca2+ release and free Ca2+ concentration. Thus, the use of even low concentrations of BDM as an excitation-contraction uncoupler must be approached with caution.

摘要

2,3-丁二酮单肟（BDM）是一种众所周知的骨骼肌和心肌收缩抑制剂。最近，人们发现BDM对肌浆网（SR）有影响。我们在洋地黄皂苷裂解的心肌细胞系统中研究了BDM对SR的影响，该系统可测量SR中积累的Ca2+。虽然BDM（30 mM）对SR Ca2+摄取没有影响（在包括Ca2+释放通道流出抑制剂的条件下），但它能诱导SR Ca2+释放（无流出抑制剂），在pCa 6.0时，SR Ca2+的最大减少量为72%。滴定显示，即使是5 mM的BDM在相同的pCa下也会导致45%的减少。此外，还发现BDM诱导的Ca2+释放程度与游离Ca2+浓度之间存在正相关。因此，即使使用低浓度的BDM作为兴奋-收缩解偶联剂也必须谨慎。