Potassium-chloride cotransport in cultured chick heart cells.
Potassium-chloride cotransport in cultured chick heart cells.
复制标题
培养鸡心脏细胞中的钾-氯化物共转运。
DOI：
10.1152/ajpcell.1985.249.3.c337
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Lieberman,M
中科院分区：
文献类型：
--
作者：
Piwnica-Worms,D;Jacob,R;Horres,CR;Lieberman,M
体外培养的鸡心脏细胞多链制备具有单向的跨膜Cl-外排，是K+外排的两倍。然而，这种心脏细胞膜的Cl-电导很低[无论细胞外K+ (K+o)如何]，这表明存在电中性的Cl-依赖转运机制。速尿（10(-3)M）将36Cl示踪剂的流出速率常数从控制值0.67降低到0.33 min-1。细胞外无Na+溶液在1分钟内耗尽细胞内Na+，对36Cl外排无显著影响。无K+o溶液加4,4'-二异硫氰基二苯乙烯-2,2'-二磺酸（DIDS; 10(-4) M）对Cl-的电化学梯度促进Cl-的损失；氯离子损失对速尿具有剂量依赖性。在133 mM K+o中培养多链，正常的细胞外Cl- (Cl-o)溶液会导致净K+和Cl-以1:1的化学计量学吸收，以及速尿敏感的体积增加；130mm细胞外胆碱或Li+不能模拟高k +o诱导的体积增加。从133 mM K+o溶液中去除Cl-o会阻止K+的吸收，并导致Cl-损失以及速尿敏感性体积减小。调节高K+o溶液中Cl-o浓度加上DIDS，使Cl-化学梯度与K+化学梯度相等，防止高K+o引起的体积变化。这些数据表明，心脏细胞膜含有速尿敏感的K+- cl -共转运机制。
The polystrand preparation of cultured chick heart cells has a unidirectional transmembrane Cl- efflux that is twice K+ efflux. However, Cl- conductance of this heart cell membrane is low [regardless of extracellular K+ (K+o)], suggesting the existence of electroneutral Cl--dependent transport mechanisms. Furosemide (10(-3) M) decreases the 36Cl tracer efflux rate constant from a control value of 0.67 to 0.33 min-1. Extracellular Na+--free solution, which depletes intracellular Na+ within 1 min, has no significant effect on 36Cl efflux. K+o-free solution plus 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 10(-4) M) promotes the loss of Cl- against the Cl- electrochemical gradient; Cl- loss is furosemide sensitive in a dose-dependent manner. Incubating polystrands in 133 mM K+o, normal extracellular Cl- (Cl-o) solution causes net K+ and Cl- uptake in a 1:1 stoichiometry as well as a furosemide-sensitive volume increase; 130 mM extracellular choline or Li+ cannot mimic this high-K+o-induced volume increase. Removal of Cl-o from 133 mM K+o solution prevents K+ uptake and causes a Cl- loss as well as a furosemide-sensitive volume decrease. Adjusting Cl-o concentrations in high-K+o solution plus DIDS, so that the Cl- chemical gradient equally opposes the K+ chemical gradient, prevents high-K+o-induced volume changes. These data suggest that the cardiac cell membrane contains a furosemide-sensitive K+-Cl- cotransport mechanism.