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钾离子诱导氯离子跨青蛙视网膜色素上皮细胞的分泌。

Potassium-induced chloride secretion across the frog retinal pigment epithelium.

作者信息

Edelman J L, Lin H, Miller S S

机构信息

School of Optometry, University of California, Berkeley 94720.

出版信息

Am J Physiol. 1994 Apr;266(4 Pt 1):C957-66. doi: 10.1152/ajpcell.1994.266.4.C957.

DOI:10.1152/ajpcell.1994.266.4.C957
PMID:8178968
Abstract

In the intact eye, a transition from light to dark increases K concentration ([K]o) from approximately 2 to 5 mM in the extracellular (subretinal) space between the photoreceptors and the retinal pigment epithelium (RPE) apical membrane. In control (HCO3/CO2) Ringer solution, 36Cl was actively absorbed across isolated bullfrog RPE (retina to choroid) at a rate of 0.31 +/- 0.02 (SE) mu eq.cm-2.h-1 (n = 15). Elevating apical [K]o from 2 to 5 mM reversed active 36Cl transport to secretion (choroid to retina), with a rate of 0.76 +/- 0.17 mu eq.cm-2.h-1. This reversal was completely inhibited by 1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) in either the apical or basal bath. In open circuit, elevating [K]o induced a similar reversal of net 36Cl flux and inhibited fluid absorption by approximately 25%. Apical Ba2+ (1 mM), decreased CO2 (5 to 1%), or increased apical bath HCO3 concentration ([HCO3]o) also caused a DIDS-inhibitable reversal of active 36Cl flux. A 10-fold reduction of apical bath Na or [HCO3]o significantly inhibited [K]o, Ba2+, and low CO2-induced Cl secretion. All of these results can be understood in terms of an intracellular pH-dependent stimulation of the basolateral membrane Cl-HCO3 exchanger.

摘要

在完整的眼睛中,从明适应转变为暗适应会使光感受器与视网膜色素上皮(RPE)顶膜之间的细胞外(视网膜下)空间中的钾离子浓度([K]o)从约2 mM增加到5 mM。在对照(HCO3/CO2)林格氏液中,36Cl以0.31±0.02(SE)μeq·cm-2·h-1的速率被主动吸收穿过分离的牛蛙RPE(从视网膜到脉络膜)(n = 15)。将顶膜[K]o从2 mM提高到5 mM会使36Cl的主动转运逆转成分泌(从脉络膜到视网膜),速率为0.76±0.17 μeq·cm-2·h-1。这种逆转在顶膜或基底浴中被1 mM的4,4'-二异硫氰基芪-2,2'-二磺酸(DIDS)完全抑制。在开路状态下,提高[K]o会引起净36Cl通量的类似逆转,并抑制液体吸收约25%。顶膜Ba2+(1 mM)、降低CO2(从5%降至1%)或增加顶膜浴中的HCO3浓度([HCO3]o)也会导致DIDS可抑制的主动36Cl通量逆转。将顶膜浴中的Na或[HCO3]o降低10倍会显著抑制[K]o、Ba2+和低CO2诱导的Cl分泌。所有这些结果都可以通过细胞内pH依赖的基底外侧膜Cl-HCO3交换器刺激来解释。

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