Rayson B M
Department of Physiology, Cornell University Medical College, New York, New York 10021.
J Biol Chem. 1993 Apr 25;268(12):8851-4.
Chronic reduction of Na+/K(+)-ATPase activity has been demonstrated in a number of cell systems to elicit a cellular homeostatic response. Over the course of this response, there is initially a transient stimulation of synthesis of new Na+/K(+)-ATPase molecules, followed by a delayed decrease in its degradation rate, eliciting an effective increase in the number of active pumps in the membrane. The resultant enhancement of pumping capacity promotes the extrusion of accumulated Na+ ions and restores the intracellular electrolyte milieu to preinsult conditions. No cellular mediators of either component of this response have previously been described. We therefore tested the possibility that changes in [Ca2+]i might contribute to the transient stimulation of synthesis observed. Indeed, an effective synthetic response to the inhibition of Na+/K(+)-ATPase by treatment with ouabain required elevated [Ca2+]i levels.
在许多细胞系统中已证实，慢性降低钠钾ATP酶活性会引发细胞内稳态反应。在该反应过程中，最初会短暂刺激新的钠钾ATP酶分子的合成，随后其降解速率延迟降低，从而有效增加膜上活性泵的数量。由此产生的泵浦能力增强促进了积累的钠离子的排出，并将细胞内电解质环境恢复到损伤前的状态。此前尚未描述过该反应任一组成部分的细胞介质。因此，我们测试了细胞内钙离子浓度的变化可能导致所观察到的合成短暂刺激的可能性。事实上，用哇巴因处理抑制钠钾ATP酶后，有效的合成反应需要升高的细胞内钙离子浓度水平。
