Yashar P R, Fransua M, Frishman W H
Department of Medicine, Cedars-Sinai Medical Center, UCLA School of Medicine, USA.
J Clin Pharmacol. 1998 May;38(5):393-401. doi: 10.1002/j.1552-4604.1998.tb04442.x.
The Na(+)-Ca2+ exchanger is a non-ATP-dependent protein that, under steady-state conditions, extrudes Ca2+ from the interior of the cell into the extracellular space via facilitated transport. The activity of the exchanger seems to be reduced in myocardial ischemia, leading to increased intracellular Ca2+ in the ischemic heart, which can result in arrhythmia, myocardial stunning, and necrosis. In contrast, congestive heart failure and myocardial hypertrophy are associated with increased exchanger activity and a decreased inotropic state. Pharmacologic agents are being developed to modulate sodium ion levels in the cell, which could enhance or reduce sodium-calcium exchange as needed in various pathophysiologic states. At this time there are no available drugs that act specifically on the Na(+)-Ca2+ exchanger itself. The exchanger has been cloned, and inhibitory peptides of the exchanger may soon be available for possible use in treatment of congestive heart failure.
钠钙交换体是一种不依赖三磷酸腺苷的蛋白质，在稳态条件下，它通过易化转运将细胞内的钙离子挤出到细胞外空间。在心肌缺血时，该交换体的活性似乎降低，导致缺血心肌细胞内钙离子增加，进而可引发心律失常、心肌顿抑和坏死。相反，充血性心力衰竭和心肌肥大与交换体活性增加及变力状态降低有关。目前正在研发可调节细胞内钠离子水平的药物，这些药物可根据不同病理生理状态的需要增强或降低钠钙交换。目前尚无专门作用于钠钙交换体本身的药物。该交换体已被克隆，其抑制性肽可能很快可用于充血性心力衰竭的治疗。
