Alabovskiĭ V V, Vinokurov A A
Vopr Med Khim. 1996 Oct-Dec;42(4):291-5.
Heart maintains a gradient for creatine under physiological conditions, so that creatine release is relatively small. Calcium depletion, addition of strophanthin or decrease of sodium concentration (till 80 mM) provoke release of creatine. Elevation of transmembrane sodium gradient by raising of extracellular sodium concentration prevented loss of creatine. The effect of elevated concentration of sodium ions was blocked by strophanthin but depended on osmolarity, because solutions with the same osmolarity that hypersodium media had no protective effect on release of creatine. A sarcolemmal mechanism of Na creatine cotransports is proposed.
在生理条件下，心脏维持肌酸梯度，使得肌酸释放相对较少。钙耗竭、加入毒毛花苷或降低钠浓度（直至80 mM）会引发肌酸释放。通过提高细胞外钠浓度升高跨膜钠梯度可防止肌酸丢失。毒毛花苷可阻断钠离子浓度升高的作用，但该作用取决于渗透压，因为与高渗钠培养基渗透压相同的溶液对肌酸释放无保护作用。提出了肌酸钠共转运的肌膜机制。
