Intracellular chloride activities in the isolated perfused shark rectal gland.

Intracellular chloride activities in the isolated perfused shark rectal gland.
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离体灌注鲨鱼直肠腺中的细胞内氯化物活动。

DOI:
10.1152/ajprenal.1983.245.5.f640
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发表时间:
1983
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Frizzell,RA
Frizzell,RA
中科院分区:
--
文献类型:
--
作者:
Welsh,MJ;Smith,PL;Frizzell,RA

文献摘要

被引文献

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离体灌注的鲨鱼直肠腺在受到腺苷3′,5′-环单磷酸腺苷(cAMP)刺激时分泌Cl。为了研究其分泌机制,我们使用Cl选择性微电极和常规(充满kcl)微电极测量细胞内Cl活性(aClc)。在非分泌条件下,基底侧膜上的电位差(psi b)为-78 m V, aClc为57 mM,比基底侧膜上电化学平衡的预测值大7倍。当灌注液中加入茶碱和8-溴- camp时,经腺电位差增加一倍,液体分泌速度增加20倍;然而,psi b和aClc都没有改变。在非分泌和分泌条件下,细胞内Cl的积累导致电化学电位差,有利于Cl通过顶细胞膜出口。aClc的恒定,尽管分泌速率的变化表明,刺激与净Cl在根尖和基底外膜上的运动等效增强有关。当受刺激的腺体灌注无钠(胆碱)林格时,分泌被消除,aClc下降到电化学平衡的预测值。这些发现表明,Cl分泌的“上坡”阶段位于基底外膜,细胞Cl积聚可能涉及继发性主动运输;也就是说,Cl的进入是由Na向内的电化学电位差驱动的。
The isolated, perfused shark rectal gland secretes Cl when stimulated with adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of secretion, we used Cl-selective and conventional (KCl-filled) microelectrodes to measure the intracellular Cl activity (aClc). Under nonsecreting conditions, the electrical potential difference across the basolateral membrane (psi b) was -78 m V and aClc was 57 mM, a value seven times greater than predicted for electrochemical equilibrium across the basolateral membrane. When theophylline and 8-bromo-cAMP were added to the perfusate, the transglandular electrical potential difference doubled and the rate of fluid secretion increased 20-fold; however, neither psi b nor aClc changed. During both nonsecreting and secreting conditions the intracellular accumulation of Cl results in an electrochemical potential difference favoring Cl exit across the apical cell membrane. The constancy of aClc despite the variation in secretion rate suggests that stimulation is associated with an equivalent enhancement of net Cl movement across both the apical and basolateral membranes. When stimulated glands were perfused with Na-free (choline) Ringer, secretion was abolished and aClc fell toward the value predicted for electrochemical equilibrium. These findings suggest that the "uphill" step in Cl secretion lies at the basolateral membrane, where cellular Cl accumulation probably involves secondary active transport; i.e., Cl entry is driven by an inwardly directed electrochemical potential difference for Na.