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机构地区:[1]北京医科大学中西医结合研究室,北京100083 [2]河北医科大学基础医学院药理教研室,石家庄050017
出 处:《中国药理学通报》1998年第S1期41-44,共4页Chinese Pharmacological Bulletin
摘 要:Ca^(2+)平衡是维持心肌细胞正常电生理活动的重要前提。在各种机制中,肌质网Ca-ATPase与肌膜Na/Ca交换蛋白对于维持胞内Ca^(2+)的平衡发挥主要作用。其中肌膜Na/Ca交换蛋白是Ca^(2+)排出胞外的主要途径,并通过调节细胞内静息状态下[Ca^(2+)]调节肌质网的[Ca(2+)]含量,从而调节心肌细胞的收缩力。少量Ca(2+)内流入胞后可触发肌质网释放大量Ca(2+)(CICR)。已证实动作电位峰电位及平台期有Ca(2+)通过Na/Ca内流,这种除极化诱导的Ca(2+)经Na/Ca内流可能是触发CICR的主要因素。总之Na/Ca交换蛋白在兴奋-收缩耦联中的作用需要重新加以评价。ABSTRACT Calcium homeostasis is of crucial importance for the function of cardial myocytes in normal electrical and mechanical processes. The sarcoplasmic reticular Ca-ATPase and the sar-colemmic Na/Ca exchanger contribute mainly to the steady state of calcium in the myoplasm. The Na/Ca exchanger serves as the principal calcium extrusion mechanism and regulates calcium content of the sarcoplasmic reticulum by regulating the resting [Ca2+]i level, through which the Na/Ca exchanger regulates the force of contraction sequentially. Very small calcium entry can trigger significant sarcoplasmic reticular calcium release (CICR). During the upstroke and plateau phasesof the action potential, There is evidence that indicates Ca2+ influx via the Na/Ca exchanger, and the depolarisation-induced calcium entry on Na/Ca exchange may contribute mainly to triggering intra-cellular calcium release. Na/Ca exchange should be reevaluated as a route through which Ca2+, as a triggering signal, enters cardiac myocyte during excitation-contraction coupling.
分 类 号:R331.38[医药卫生—人体生理学]
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