CELL-VOLUME REGULATION BY TROUT ERYTHROCYTES - CHARACTERISTICS OF THE TRANSPORT-SYSTEMS ACTIVATED BY HYPOTONIC SWELLING

被引:107
作者
GARCIAROMEU, F
COSSINS, AR
MOTAIS, R
机构
[1] Laboratoire Jean Maetz, Département de Biologie Cellulaire et Moléculaire, Commissariat à l'Energie Atomique, Villefranche-Sur-Mer
来源
JOURNAL OF PHYSIOLOGY-LONDON | 1991年 / 440卷
关键词
D O I
10.1113/jphysiol.1991.sp018724
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
1. An osmolality reduction of the suspending medium leads to osmotic swelling of trout erythrocytes, which is followed by a volume readjustment towards the original level. The regulatory volume decrease (RVD) was not complete after 1 h. 2. During RVD the cells lost K+ and Cl- but gained Na+. This entry of Na+, which is about half the K+ loss, explains the incomplete volume recovery (it was complete when Na+ was replaced by impermeant N-methyl-D-glucamine). The cells also lose large quantities of taurine, which accounts for about 53% of the volume recovery. In addition RVD is accompanied by the activation of a pathway allowing some large organic cations which are normally impermeant, such as choline or tetramethylammonium, to rapidly penetrate the cells. 3. The swelling-activated K+ loss is not significantly affected by replacement of Cl- by NO3-, indicating that K+ moves through a Cl--independent K+ pathway. Furosemide, DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid) and niflumic acid inhibit the K+ loss. From experiments performed in high-K+-containing media, it appears that these compounds block the K+ flux, not by inhibiting Cl- movements but by interfering with the K+ pathway. 4. All the volume-activated pathways (K+, Na+, taurine, choline) are fully inhibited by furosemide and by inhibitors of the anion exchanger such as DIDS and niflumic acid. The concentration required for 50% inhibition (IC50) of both inorganic cations and taurine appears to be similar. It is proposed that DIDS interacts with a unique target which controls all the volume-sensitive transport systems.
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页码:547 / 567
页数:21
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