Howlett S E, Gordon T
Biochem Pharmacol. 1987 Aug 15;36(16):2653-9. doi: 10.1016/0006-2952(87)90547-8.
Progressive cardiac cell necrosis in the dystrophic hamster may be related to intracellular calcium overload, particularly as necrosis is prevented by treatment with calcium channel antagonists. Calcium overload could arise as a consequence of an imbalance in calcium influx, efflux and/or sequestration. The possibility that increased numbers of calcium channels in myopathic cells leads to excessive calcium influx has been studied by assaying the number of [3H]nitrendipine [( 3H]NTP) binding sites in cardiac muscle preparations. Crude homogenate and partially-purified ventricular muscle preparations from 60-day-old normal and genetically dystrophic hamsters were compared in this study. The results of equilibrium binding studies showed that, in both crude and partially-purified membrane preparations, the affinity and the maximum number of [3H]NTP binding sites in normal muscle were not significantly different from those measured in dystrophic muscle. For the homogenate preparation, the KD values were 0.07 +/- 0.01 and 0.08 +/- 0.01 nM for normal and dystrophic tissues, respectively, and the Bmax values were 62 +/- 6 and 73 +/- 6 fmol/mg protein for normal and dystrophic preparations respectively. These data show that a simple increase in the number of [3H]NTP binding sites is unlikely to account for calcium overload in the cardiomyopathic hamster.
营养不良性仓鼠中进行性心肌细胞坏死可能与细胞内钙超载有关，尤其是当用钙通道拮抗剂治疗可预防坏死时。钙超载可能是钙流入、流出和/或螯合失衡的结果。通过测定心肌制剂中[3H]尼群地平[（3H）NTP]结合位点的数量，研究了肌病细胞中钙通道数量增加导致钙过度流入的可能性。本研究比较了60日龄正常和遗传性营养不良仓鼠的粗匀浆和部分纯化的心室肌制剂。平衡结合研究结果表明，在粗制和部分纯化的膜制剂中，正常肌肉中[3H]NTP结合位点的亲和力和最大数量与营养不良肌肉中测得的无显著差异。对于匀浆制剂，正常和营养不良组织的KD值分别为0.07±0.01和0.08±0.01 nM，正常和营养不良制剂的Bmax值分别为62±6和73±6 fmol/mg蛋白。这些数据表明，[3H]NTP结合位点数量的简单增加不太可能解释心肌病仓鼠中的钙超载。
